Arya Mani
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Research Summary
My laboratory is engaged in system biology approaches to investigate cardiovascular diseases. We leverage modern techniques of functional genomics, epigenetics, transcriptomics, proteomics, gene editing and model-driven experimentation to understand the underlying causes of atherosclerosis and metabolic syndrome and discover therapeutic targets. Our work involves population and family-based genetic studies, high throughput sequencing to identify disease genes, with a focus on coronary artery disease (CAD) and metabolic syndrome (MetS). We then proceed to characterize the identified genes in vivo and in vitro. By recruiting more than thousand kindreds with early onset CAD and multiple metabolic risk factors for genetics and metabolic studies we have been able to map, identify and characterize a dozen of human disease genes for CAD and MetS, which have been reported in leading journals such as Nat Genet, Science, NEJM, Cell Metab, JCI, PNAS, AJHG, etc. We were the first group to show the role of Wnt signaling in atherosclerosis and the first to establish a genetic link between exocrine and endocrine pancreas in pathogenesis of diabetes. Most recently, we have established techniques of high throughput gene editing and multiple parallel reporter assays in my laboratory and have successfully mapped the regulatory landscape of a number of GWAS disease genes. Subsequent molecular and physiological studies in human mutation carriers and animal models have allowed us to unravel novel functions of the identified genes, to delineate their cognate pathways and to discover new targets for pharmaceutical intervention. These groundbreaking achievements have made us one of the leading laboratories in investigation of metabolic syndrome. We have developed expertise in in vivo investigation of lipid and glucose metabolism, insulin secretion and sensitivity, and vascular biology and in human physiological studies, leading to discovery of attractive drug targets that have been either patented or being investigated for their utility in treatment of fatty liver disease and diabetes in 2 clinical trials in the outlier populations of Fars/Iran. One of our groundbreaking discoveries was the identification of founder mutations in the DYRK1B gene, underlying atherosclerosis, metabolic syndrome, and fatty liver disease. The encoded protein is upregulated in human steatosis (NASH). Our studies in mice have shown that this upregulation results in mTOR activation, lipogenesis and development of NASH and dyslipidemia. Strikingly, knockdown of Dyrk1b is protective against these traits, motivating further investigations to characterize the protein as an attractive therapeutic target. One of our recent groundbreaking discoveries was the identification of novel loss of function mutations in a gene encoding the pancreatic exocrine elastase Cela2a in patients with diabetes, CAD and MetS traits, including obesity, hypertension, hypertriglyceridemia, NAFLD (OMIM: AOMS4). The characterization of this protein in vivo has shown that it widely expressed in different tissues and circulates in the blood, its levels rise after food intake in humans and stimulates insulin secretion and sensitivity and inhibits platelet aggregation. We are now fully characterizing this protein and evaluating its utility as a drug target for diabetes, dyslipidemia, and fatty liver disease. These discoveries are the results of lengthy and high risk studies, which would have not been accomplished without the R35 grant mechanism and the hard work and devotion of students, residents , fellows and visiting scholars in my laboratory, many of whom have gone to establish their own labs, or join the industry. Alone 7 former lab members have joined academia over the past 5 years and 11 a pursuing a career in research as trainees.
Sample publications:
1. (AHA Young Investigator award Finalist) Fatemehsadat Esteghamat, James Samuel Broughton, Emily Smith, Rebecca Cardone, Tarun Tyagi, Mateus Guerra, András Szabó, , Nelson Ugwu, Mitra Mani, Bani Azari, Gerald Kayingo, Sunny Chung, Mohsen Fathzadeh, Ephraim Weiss, Jeffrey Bender, Shrikant Mane5, Richard Lifton, Adebowale Adeniran, Michael Nathanson, Fred Gorelick, John Hwa, Miklós Sahin-Tóth, Renata Belfort-DeAguiar, Richard Kibbey, Arya Mani,. CELA2A mutations predispose to early-onset atherosclerosis and metabolic syndrome and affect plasma insulin and platelet activation. Nat Genet, 2019, 1233-1243. PMID:31358993
2. (Recommended by F1000Prime/AHA Young Investigator Award Finalist) Keramati AR, Fathzadeh M, Singh R, Lin A, Faramarzi S, Choi M, Mane S, Kasae M, Babaee Bigi, Malekzadeh R, Hosseinian Babaie M, Lifton RP, and Mani A. A form of the metabolic syndrome associated with mutations in DYRK1B. NEJM, 2014 ;370(20):1909-19, PMID: 24827035
3. (Editors’ choice) Mani A (co-corresponding author), Radhakrishnan J, Wang H, Mani A, Mani MA, Nelson-Williams C, Carew KS, Mane S, Najmabadi H, Wu D, Lifton RP. LRP6 Mutation in a Family with Early Coronary Disease and Metabolic Risk Factors. Science 2007;315:1278-82. PMC2945222
Extensive Research Description
1. Hyperlipidemia and fatty liver disease
Wnt coreceptor LDL receptor-related protein 6 (LRP6) gene was the very first monogenic cause of coronary artery disease (OMIM: ADCAD2) and MetS (Science 2007), which we discovered in our lab. Genotype phenotype correlation showed that the mutations impact a number of metabolic phenotypes, including hypercholesterolemia and nonalcoholic fatty liver disease (NAFLD). This discovery caused a paradigm shift by establishing a causal link between impaired LRP6 /Wnt signaling and CAD and its associated metabolic traits. Having unique access to the study populations, we investigated the role of LRP6 in regulation of cholesterol uptake in primary human cells and tissues and demonstrated its role in clathrin-mediated LDLR endocytosis. Mice generated in our lab with the human LRP6 mutation (LRP6R611C) exhibited elevated plasma LDL and TG levels and developed steatohepatitis and steatofibrosis. The molecular dissection of the disease pathways showed that the LRP6 mutation triggers hepatic de-novo lipogenesis (DNL) via TCF7L2-dependent activation of mTOR nutrient sensing pathway. These traits were rescued by in vivo administration of rmWnt3a, identifying Wnt pathways as an attractive therapeutic target against NASH. The investigation of a large, inbred population with extremely high prevalence obesity, MetS and NAFLD led to the discovery of founder mutations in DYRK1B gene as the second monogenic cause of MetS and NAFLD. Further studies revealed that DYRK1B protein levels are increased in the liver of most patients with NASH and in mice fed with a high calorie diet. Strikingly, the induction of hepatic Dyrk1b in mice on chow diet enhanced de novo lipogenesis (DNL), fatty-acid uptake, and TAG secretion and caused NASH and hyperlipidemia by activating mTORC2 pathway. Conversely, knockdown of Dyrk1b was protective against these traits. These findings identify DYRK1B as an attractive target for NAFLD, motivating further investigations into the utility of Dyrk1a/b proteins as attractive drug targets for NAFLD.
- Neha Bhat, Anand Narayanan, Mohsen Fathzadeh, Mario Kahn, Leigh Goedeke, Noemi Vila, Arpita Neogi, Henry N Ginsberg, Dhanpat Jain, Carlos Fernandez-Hernando, Gerald I Shulman, Arya Mani. Dyrk1b is a novel therapeutic target for nonalcoholic steatohepatitis (NASH) and insulin resistance J Clin Invest. 2021Dec 2:e153724. PMID: 34855620
- Wang S, Song K, Srivastava R, Dong C, Go GW, Li N1, Iwakiri Y, Mani A. Nonalcoholic fatty liver disease induced by noncanonical Wnt and its rescue by Wnt3a. FASEB 2015 PMID: 25917329
- Go GW, Srivastava R, Hernandez-Ono A, Gang G, Smith SB, Carmen J, Booth CJ, Ginsberg HN, and Mani A. The Combined Hyperlipidemia Caused by Impaired Wnt-LRP6 signaling is reversed by Wnt3a Rescue. Cell Metab. 2014;19(2):209-220. PMID: 24506864
- Liu W, Mani S, Davis NR, Sarrafzadegan N, Kavathas PB, Mani A. Mutation In EGFP Domain of LDL Receptor-Related Protein 6 Impairs Cellular LDL Clearance. Circulation Research 2008;103(11):1280-1288. PMID:18948618
2. Atherosclerosis Our lab was the first to discover the role of altered Wnt signaling in atherosclerosis. In collaboration with a team of cardiothoracic surgeons at Yale we showed the dramatic increase in expression of Wnt coreceptor LRP6 in human atherosclerotic coronary arteries as a response to injury. By dissecting the molecular pathways in human VSMCs, we were able to show that LRP6 forms a complex with PDGFR-β, enhances its lysosomal degradation, increases VSMC differentiation and prevents excessive proliferation. These functions were severely impaired by LRP6 mutations resulting in the activation of noncanonical Wnt signaling. Our findings implicated LRP6 as a critical modulator of PDGF-dependent regulation of cell cycle in VSMC and showed that loss of this function contributes to development of early onset atherosclerosis. One of the most exciting developments in our lab was the generation of a novel coronary artery disease mouse model. Mice carrying the human LRP6R611C mutation displayed dramatic obstructive CAD on high fat diet and exhibited an accelerated atherosclerotic burden on LDLR knockout background. The dissection of disease pathways revealed that impaired LRP6 activity triggers non-canonical Wnt signaling, culminating in diminished TCF7L2 and increased activation of PDGF signaling. Strikingly, Wnt3a administration to LRP6R611C mice improved the activity of LRP6 and its downstream signaling pathway, led to TCF7L2-dependent VSMC differentiation, and rescued post carotid injury neointima formation. Accordingly, we showed in a separate study that mice deficient for TCF7L2 develop wire injury-induced carotid intimal hyperplasia, while the overexpression of TCF7L2 is protective against it and can rescue post-injury intimal hyperplasia of LRP6R611C mice. These findings underscored the critical role of intact Wnt signaling in maintaining the normal structure of the vessel wall, established a causal link between impaired LRP6/TCF7L2 activities and arterial disease and identified Wnt/TCF7L2 as an attractive target for the treatment of CAD. Motivated by these remarkable findings, we are currently working with the industry to study the effect of Wnt-inhibitors antagonists to treat intimal hyperplasia.
- Keramati AR, Singh R, Lin A, Faramarzi S, Ye Z, Mane S, Tellides G, Lifton RP, and Mani A. Wild-type LRP6 inhibits, whereas atherosclerosis-linked LRP6R611C increases PDGF-dependent vascular smooth muscle cell proliferation. Proc Natl Acad Sci U S A ,2011, 108(5):1914-8, PMC3033290.
- Srivastava R, Zhang J, Go GW, Narayanan A, Nottoli TP, Mani A. Impaired LRP6-TCF7L2 activity enhances smooth muscle cell plasticity and causes coronary artery disease. Cell Reports,2015.13(4):746-59 PMID: 26489464
c. Srivastava R, Rolyan H, Xie Y, Li N, Bhat N, Hong L, Esteghamat F, Adeniran A, Geirsson A, Zhang J, Ge G, Nobrega M, Martin KA, Mani A. TCF7L (Transcription Factor 7-Like ) Regulation of GATA6 (GATA-Binding Protein 6)-Dependent and -Independent Vascular Smooth Muscle Cell Plasticity and Intimal Hyperplasia Arterioscler Thromb Vasc Biol. 2019 Feb;39(2):250-262 PMID:30567484
3. Molecular Genetics of Diabetes and Insulin Resistance The molecular mechanisms underlying insulin resistance are poorly understood. Our studies using different genetic mouse models have revealed that altered function of skeletal muscle, endothelial cells, and hepatocytes can all impair glucose tolerance. Our human genetic studies had established a causal link between missense mutations in LRP6 and DYRK1B genes and type 2 diabetes. LRP6 mutation carriers exhibited hyperinsulinemia and reduced insulin sensitivity compared to noncarrier relatives in response to oral glucose ingestion, which correlated with a significant decline in the skeletal muscle expression of the insulin receptor and canonical insulin signaling activity. Further investigations showed that the LRP6(R611C) mutation diminishes TCF7L2-dependent transcription of the IR while it triggers mTORC1-dependent IRS1/2-phosphorylation and inactivation. We have recently shown Dyrk1b gain of function causes insulin resistance by increasing plasma membrane sn-1,2-diacylglyerol levels and PKCε-mediated IRKT1150 phosphorylation in the liver, which results in impaired activation of hepatic insulin signaling and reduced hepatic glycogen storage. In a separate study we showed that the loss of Apelin in the endothelial cell increases fatty acid uptake and causes insulin resistance.
- Liu W, Singh R, Choi CS, Lee HY, Keramati AR, Samuel VT, Lifton RP, Shulman GI, Mani A. Low density lipoprotein (ldl) receptor-related protein 6 (lrp6) regulates body fat and glucose homeostasis by modulating nutrient sensing pathways and mitochondrial energy expenditure. J Biol Chem. 2012;287:7213-7223PMC3293520
- (featured article) Singh R, De Aguiar RB, Naik S, Mani S, Ostadsharif K, Wencker D, Sotoudeh M, Malekzadeh R, Sherwin RS, Mani A. Lrp6 enhances glucose metabolism by promoting tcf7l2-dependent insulin receptor expression and igf receptor stabilization in humans. Cell Metab. 2013;17:197-209PMC3589523
- Cheol Hwangbo, Jingxia Wu, Irinna Papangeli, Takaomi Adachi, Bikram Sharma, Saejeong Park, Lina Zhao, Hyekyung Ju, Gwang-woong Go,1 Guoliang Cui, Mohammed I.N. Ahmed, Judith Job, Rajadas, Stephanie L. Kwei, Ming O. Li, Alan R. Morrison, Thomas Quertermous, Arya Mani, Kristy Red-Horse, Hyung J. Chun, Endothelial APLNR regulates tissue fatty acid uptake and is essential for apelin’s glucose lowering effects Sci Transl Med. 2017 Sep 13;9. PMID:28904225
- Neha Bhat, Anand Narayanan, Mohsen Fathzadeh, Mario Kahn, Leigh Goedeke, Noemi Vila, Arpita Neogi, Henry N Ginsberg, Dhanpat Jain, Carlos Fernandez-Hernando, Gerald I Shulman, Arya Mani. Dyrk1b is a novel therapeutic target for nonalcoholic steatohepatitis (NASH) and insulin resistance J Clin Invest. 2021Dec 2:e153724. PMID: 34855620
4. The molecular genetics of patent ductus arteriosus My laboratory has been interested in the pathogenesis of patent ductus arteriosus as a gateway to the discovery of pathways that maintain patency of arterial lumens. We have mapped and identified disease genes for syndromic and nonsyndromic, autosomal dominant and recessive patent ductus arteriosus. The in vivo and in vitro characterization of disease genes has led to discovery of genetic networks that alter neural crest cell migration and differentiation. Specifically, we discovered that increased Wnt activation causes the patency of the ductus by impairing smooth muscle cell proliferation, a process that is sharply opposite to the pathogenesis of CAD in mice with defective Wnt coreceptor LRP6. This finding supports our earlier discoveries, implicating Wnt signaling in vascular remodeling.
- Lingjuan Hong, Na Li, Victor Gasque, Sameet Mehta, lupeng ye, yinyu wu, jinyu li, Andreas Gewies, Jürgen Ruland, Karen Hirschi, Anne Eichmann, Caroline Hendry, David van dijk, Arya Mani. Prdm6 controls heart development by regulating neural crest cell specification and migration. JCI Insight (in press)
- Li N, Subrahmanyan L, Smith E, Yu X, Zaidi,S, Choi M, Mane S, Nelson-Williams C, Bahjati M, Kazemi M, Hashemi M, Fathzadeh M, Narayanan A, Tian L, Montazeri F Mani M, Begleiter ML, Coon BG, Lynch HT, Olson EN, Zhao Ho, Ruland J, Lifton RP, and Mani A. Mutations in the histone modifier PRDM6 are associated with isolated nonsyndromic patent ductus arteriosus. Am J Hum Genet. 2016; 98(6):1082-91PMID: 27181681
- Mani A, Radhakrishnan J, Farhi A, Carew KS, Warne CA, Nelson-Williams C, Day RW, Pober B, State MW, Lifton RP. Syndromic patent ductus arteriosus: evidence for haplo insufficient TFAP2B mutations and identification of a linked sleep disorder. Proc Natl Acad Sci U S A 2005;102: 2975-2979. PMC549488
- Mani A, Meraji SM, Houshyar R, Radhakrishnan J, Mani A, Ahangar M Rezaie TM, Taghavinejad MA, Broumand B, Zhao H, C. Nelson-Williams C, Lifton R. Finding genetic contributions to sporadic disease: A recessive locus at 12q24 commonly contributes to patent ductus arteriosus. Proc Natl Acad Sci U S A 2002;99:15054-15059. PMC137543
5. Genetics of Atrial fibrillation (AF) and arrhythmias
As the director of the Cardiovascular Genetics program, I have access to a large number of outlier kindreds with rare familial cardiovascular disorders. This has provided us with a unique opportunity to discover novel genes for diseases of the heart rhythm. The strong relationship between cardiac arrhythmias and atherosclerosis and metabolic syndrome in particular drives our interest. Our investigations resulted recently in identification of the first disease gene for slow atrial fibrillation and the establishment of its link to stroke.
- Abou Ziki MD, Seidelmann SB, Smith E, Atteya G, Jiang Y, Fernandes RG, Marieb MA, Akar JG, Mani A. Deleterious protein-altering mutations in the SCN10A voltage-gated sodium channel gene are associated with prolonged QT. Clin Genet. 2018 ;93(4):741-75; PMID: 28407228
- Seidelmann SB, Smith E, Subrahmanyan L, Dykas D, Abou Ziki MD, Azari B, Hannah-Shmouni F, Jiang Y, Akar JG, Marieb M, Jacoby D, Bale AE, Lifton RP, Arya Mani. The Application of Whole Exome Sequencing in the Clinical Diagnosis and Management of Inherited Cardiovascular Diseases in Circ: Cardiovasc Genet 2017 Feb;10(1):e001573. doi: 10.116, PMID: 28087566 (editor’s Choice) Abou Ziki, M; Bhat, N; Neogi, A; abboud JM; Chouairi SF; Driscoll T; Ugwu, Nelson N; Ya, Liu; Smith E; Schwartz, M; Akar, J; Mani, A . Epistatic interaction of PDE4DIP and DES mutations in familial atrial fibrillation with slow conduction. Hum Mutat. 2021;42(10):1279-1293.PMID: 34289528Adults.
Coauthors
Research Interests
Cardiology; Genetics; Heart; Heart Defects, Congenital; Metabolic Syndrome; Lipid Metabolism Disorders; Hyperlactatemia
Research Images
Selected Publications
- Dysregulation of Lipid and Glucose Metabolism in Nonalcoholic Fatty Liver DiseaseBhat N, Mani A. Dysregulation of Lipid and Glucose Metabolism in Nonalcoholic Fatty Liver Disease Nutrients 2023, 15: 2323. PMID: 37242206, PMCID: PMC10222271, DOI: 10.3390/nu15102323.
- A systems biology approach identifies the role of dysregulated PRDM6 in the development of hypertensionGunawardhana K, Hong L, Rugira T, Uebbing S, Kucharczak J, Mehta S, Karunamuni D, Cabera-Mendoza B, Gandotra N, Scharfe C, Polimanti R, Noonan J, Mani A. A systems biology approach identifies the role of dysregulated PRDM6 in the development of hypertension Journal Of Clinical Investigation 2023, 133: e160036. PMID: 36602864, PMCID: PMC9927944, DOI: 10.1172/jci160036.
- A Form of Metabolic-Associated Fatty Liver Disease Associated with a Novel LIPA VariantAnushiravani A, Jafari Khamirani H, Mohamadkhani A, Mani A, Dianatpour M, Malekzadeh R. A Form of Metabolic-Associated Fatty Liver Disease Associated with a Novel LIPA Variant Archives Of Iranian Medicine 2023, 26: 86-91. DOI: 10.34172/aim.2023.14.
- Major Adverse Limb Events Among Patients with Premature Peripheral Artery Disease Compared with Those at the Common Age Undergoing Revascularization in the Vascular Quality InitiativeKim TI, Loh S, DeWan A, Murray M, Mojibian H, Mani A, Mena-Hurtado C, Ochoa Chaar CI. Major Adverse Limb Events Among Patients with Premature Peripheral Artery Disease Compared with Those at the Common Age Undergoing Revascularization in the Vascular Quality Initiative Annals Of Vascular Surgery 2022, 87: 188-197. PMID: 35926786, DOI: 10.1016/j.avsg.2022.07.007.
- Escalation of Antithrombotic Therapy in Patients With Premature Peripheral Artery Disease Undergoing Lower Extremity RevascularizationKim T, DeWan A, Murray M, Wang H, Mani A, Mena-Hurtado C, Guzman R, Chaar C. Escalation of Antithrombotic Therapy in Patients With Premature Peripheral Artery Disease Undergoing Lower Extremity Revascularization Journal Of Vascular Surgery 2022, 75: e281. DOI: 10.1016/j.jvs.2022.03.640.
- Abstract 554: The Association Of Multiple Variants In The TNXB Gene With Vascular Aneurysms And DissectionsNeogi A, Towne M, Dykas D, Parsa N, Attar A, FATHZADEH M, Bale A, Mani A. Abstract 554: The Association Of Multiple Variants In The TNXB Gene With Vascular Aneurysms And Dissections Arteriosclerosis Thrombosis And Vascular Biology 2022, 42: a554-a554. DOI: 10.1161/atvb.42.suppl_1.554.
- Complex regulation of fatty liver diseaseGinsberg HN, Mani A. Complex regulation of fatty liver disease Science 2022, 376: 247-248. PMID: 35420931, PMCID: PMC9619413, DOI: 10.1126/science.abp8276.
- PDE4DIP in health and diseasesMani A. PDE4DIP in health and diseases Cellular Signalling 2022, 94: 110322. PMID: 35346821, PMCID: PMC9618167, DOI: 10.1016/j.cellsig.2022.110322.
- Sugar, Fat, and YAP: A Recipe for Vascular StiffnessMani A, Hwa J, Martin KA. Sugar, Fat, and YAP: A Recipe for Vascular Stiffness Circulation Research 2022, 130: 868-870. PMID: 35298300, PMCID: PMC9112226, DOI: 10.1161/circresaha.122.320880.
- TCF7L2 transcriptionally regulates Fgf15 to maintain bile acid and lipid homeostasis through gut‐liver crosstalkBhat N, Esteghamat F, Chaube BK, Gunawardhana K, Mani M, Thames C, Jain D, Ginsberg HN, Fernandes‐Hernando C, Mani A. TCF7L2 transcriptionally regulates Fgf15 to maintain bile acid and lipid homeostasis through gut‐liver crosstalk The FASEB Journal 2022, 36: e22185. PMID: 35133032, PMCID: PMC9624374, DOI: 10.1096/fj.202101607r.
- Echocardiography Fails to Detect an Extensive Aortic Root Abscess in a Patient with Infective Endocarditis: A Case ReportZogg CK, Avesta A, Bonde PN, Mani A. Echocardiography Fails to Detect an Extensive Aortic Root Abscess in a Patient with Infective Endocarditis: A Case Report European Heart Journal - Case Reports 2022, 6: ytac032-. PMID: 35295731, PMCID: PMC8922699, DOI: 10.1093/ehjcr/ytac032.
- Prdm6 controls heart development by regulating neural crest cell differentiation and migrationHong L, Li N, Gasque V, Mehta S, Ye L, Wu Y, Li J, Gewies A, Ruland J, Hirschi KK, Eichmann A, Hendry C, van Dijk D, Mani A. Prdm6 controls heart development by regulating neural crest cell differentiation and migration JCI Insight 2022, 7: e156046. PMID: 35108221, PMCID: PMC8876496, DOI: 10.1172/jci.insight.156046.
- Dyrk1b promotes hepatic lipogenesis by bypassing canonical insulin signaling and directly activating mTORC2 in miceBhat N, Narayanan A, Fathzadeh M, Kahn M, Zhang D, Goedeke L, Neogi A, Cardone RL, Kibbey RG, Fernandez-Hernando C, Ginsberg HN, Jain D, Shulman G, Mani A. Dyrk1b promotes hepatic lipogenesis by bypassing canonical insulin signaling and directly activating mTORC2 in mice Journal Of Clinical Investigation 2022, 132: e153724. PMID: 34855620, PMCID: PMC8803348, DOI: 10.1172/jci153724.
- Lower Extremity Revascularization Among Patients With Premature Peripheral Artery Disease Compared To Patients At The Common Age Of Presentation In The Vascular Quality InitiativeKim T, Loh S, Dewan A, Murray M, Mojibian H, Mani A, Mena-Hurtado C, Chaar C. Lower Extremity Revascularization Among Patients With Premature Peripheral Artery Disease Compared To Patients At The Common Age Of Presentation In The Vascular Quality Initiative Annals Of Vascular Surgery 2022, 79: 400-401. DOI: 10.1016/j.avsg.2021.12.049.
- Does Opium Consumption Have Shared Impact on Atherosclerotic Cardiovascular Disease and Cancer?Masoudkabir F, Malekzadeh R, Yavari N, Zendehdel K, Mani A, Vasheghani-Farahani A, Ignaszewski A, Toma M, Roayaei P, Turk-Adawi K, Sarrafzadegan N. Does Opium Consumption Have Shared Impact on Atherosclerotic Cardiovascular Disease and Cancer? Archives Of Iranian Medicine 2022, 25: 50-63. PMID: 35128912, DOI: 10.34172/aim.2022.08.
- Abstract 14231: The Role of Altered Notch-Sox9-Hapln1 Signaling in the Pathogenesis of Bicuspid Aortic ValveGhazizadeh Z, Liu Y, Ugwu N, Adeniran A, Neogi A, Mani A. Abstract 14231: The Role of Altered Notch-Sox9-Hapln1 Signaling in the Pathogenesis of Bicuspid Aortic Valve Circulation 2021, 144: a14231-a14231. DOI: 10.1161/circ.144.suppl_1.14231.
- Dyrk1b promotes autophagy during skeletal muscle differentiation by upregulating 4e-bp1Bhat N, Narayanan A, Fathzadeh M, Shah K, Dianatpour M, Abou Ziki MD, Mani A. Dyrk1b promotes autophagy during skeletal muscle differentiation by upregulating 4e-bp1 Cellular Signalling 2021, 90: 110186. PMID: 34752933, PMCID: PMC8712395, DOI: 10.1016/j.cellsig.2021.110186.
- How Are Epigenetic Modifications Related to Cardiovascular Disease in Older Adults?Gharipour M, Mani A, Baghbahadorani M, de Souza Cardoso CK, Jahanfar S, Sarrafzadegan N, de Oliveira C, Silveira EA. How Are Epigenetic Modifications Related to Cardiovascular Disease in Older Adults? International Journal Of Molecular Sciences 2021, 22: 9949. PMID: 34576113, PMCID: PMC8470616, DOI: 10.3390/ijms22189949.
- B-AB13-03 NOVEL ROLE OF PDE4DIP IN FAMILIAL ATRIAL FIBRILLATION WITH SLOW VENTRICULAR RESPONSEZiki M, Bhat N, Neogi A, Abboud J, Chouairi S, Ugwu N, Driscoll T, Liu Y, Smith E, Schwartz M, Akar J, Mani A. B-AB13-03 NOVEL ROLE OF PDE4DIP IN FAMILIAL ATRIAL FIBRILLATION WITH SLOW VENTRICULAR RESPONSE Heart Rhythm 2021, 18: s26. DOI: 10.1016/j.hrthm.2021.06.078.
- Epistatic interaction of PDE4DIP and DES mutations in familial atrial fibrillation with slow conductionZiki M, Bhat N, Neogi A, Driscoll TP, Ugwu N, Liu Y, Smith E, Abboud JM, Chouairi S, Schwartz MA, Akar JG, Mani A. Epistatic interaction of PDE4DIP and DES mutations in familial atrial fibrillation with slow conduction Human Mutation 2021, 42: 1279-1293. PMID: 34289528, PMCID: PMC8434967, DOI: 10.1002/humu.24265.
- Association of vitamins, minerals, and lead with lipoprotein(a) in a cross-sectional cohort of US adults.Brandt EJ, Brandt DJ, Desai NR, Spatz ES, Nasir K, Mani A. Association of vitamins, minerals, and lead with lipoprotein(a) in a cross-sectional cohort of US adults. International Journal For Vitamin And Nutrition Research 2021, 93: 99-110. PMID: 34024154, PMCID: PMC8964024, DOI: 10.1024/0300-9831/a000709.
- The significance of plasma collagen degradation products as biomarkers for advanced hypertensive heart diseaseMani K, Mani A. The significance of plasma collagen degradation products as biomarkers for advanced hypertensive heart disease Journal Of Clinical Hypertension 2021, 23: 1017-1019. PMID: 33932079, PMCID: PMC8357153, DOI: 10.1111/jch.14205.
- Wnt Signaling Cascades and Their Role in Coronary Artery Health and DiseaseWeerackoon N, Gunawardhana KL, Mani A. Wnt Signaling Cascades and Their Role in Coronary Artery Health and Disease Journal Of Cellular Signaling 2021, 2: 52-62. PMID: 33969358, PMCID: PMC8098721, DOI: 10.33696/signaling.2.035.
- Identification of homozygous mutations for hearing lossDianatpour M, Smith E, Hashemi SB, Farazifard MA, Nezafat N, Razban V, Mani A. Identification of homozygous mutations for hearing loss Gene 2021, 778: 145464. PMID: 33524517, PMCID: PMC7987747, DOI: 10.1016/j.gene.2021.145464.
- A meta-analysis of microRNA expression profiling studies in heart failureGholaminejad A, Zare N, Dana N, Shafie D, Mani A, Javanmard SH. A meta-analysis of microRNA expression profiling studies in heart failure Heart Failure Reviews 2021, 26: 997-1021. PMID: 33443726, DOI: 10.1007/s10741-020-10071-9.
- The pleiotropic effect of a deleterious DES mutation in familial atrial fibrillation and the role of PDE4DIP as a genetic modifier for heart blockAbou Ziki M, Akar J, Neogi A, Abboud J, Choueiri S, Driscoll T, Bhat N, Ugwu N, Liu Y, Smith E, Mani A. The pleiotropic effect of a deleterious DES mutation in familial atrial fibrillation and the role of PDE4DIP as a genetic modifier for heart block European Heart Journal 2020, 41 DOI: 10.1093/ehjci/ehaa946.0330.
- The role of Wnt signalling in development of coronary artery disease and its risk factorsLiu Y, Neogi A, Mani A. The role of Wnt signalling in development of coronary artery disease and its risk factors Open Biology 2020, 10: 200128. PMID: 33081636, PMCID: PMC7653355, DOI: 10.1098/rsob.200128.
- Lipoprotein(a) levels and association with myocardial infarction and stroke in a nationally representative cross-sectional US cohortBrandt EJ, Mani A, Spatz ES, Desai NR, Nasir K. Lipoprotein(a) levels and association with myocardial infarction and stroke in a nationally representative cross-sectional US cohort Journal Of Clinical Lipidology 2020, 14: 695-706.e4. PMID: 32739333, PMCID: PMC7641964, DOI: 10.1016/j.jacl.2020.06.010.
- Association of Serum Vitamins, Minerals, and Heavy Metals with Lipoprotein(a)Brandt E, Brandt D, Desai N, Spatz E, Mani A, Nasir K. Association of Serum Vitamins, Minerals, and Heavy Metals with Lipoprotein(a) Journal Of Clinical Lipidology 2020, 14: 560. DOI: 10.1016/j.jacl.2020.05.029.
- EPIDEMIOLOGY OF LIPOPROTEIN(A) AND ASSOCIATION WITH MYOCARDIAL INFARCTION AND STROKE IN A NATIONALLY REPRESENTATIVE COHORTBrandt E, Mani A, Spatz E, Desai N, Nasir K. EPIDEMIOLOGY OF LIPOPROTEIN(A) AND ASSOCIATION WITH MYOCARDIAL INFARCTION AND STROKE IN A NATIONALLY REPRESENTATIVE COHORT Journal Of The American College Of Cardiology 2020, 75: 3669. DOI: 10.1016/s0735-1097(20)34296-0.
- Global longitudinal strain imaging and its utility in assessing risk in early stages of hypertensionMani A. Global longitudinal strain imaging and its utility in assessing risk in early stages of hypertension Journal Of Clinical Hypertension 2019, 21: 1711-1712. PMID: 31553521, PMCID: PMC8030360, DOI: 10.1111/jch.13703.
- CELA2A mutations predispose to early-onset atherosclerosis and metabolic syndrome and affect plasma insulin and platelet activationEsteghamat F, Broughton JS, Smith E, Cardone R, Tyagi T, Guerra M, Szabó A, Ugwu N, Mani MV, Azari B, Kayingo G, Chung S, Fathzadeh M, Weiss E, Bender J, Mane S, Lifton RP, Adeniran A, Nathanson MH, Gorelick FS, Hwa J, Sahin-Tóth M, Belfort-DeAguiar R, Kibbey RG, Mani A. CELA2A mutations predispose to early-onset atherosclerosis and metabolic syndrome and affect plasma insulin and platelet activation Nature Genetics 2019, 51: 1233-1243. PMID: 31358993, PMCID: PMC6675645, DOI: 10.1038/s41588-019-0470-3.
- TCF7L2 (Transcription Factor 7-Like 2) Regulation of GATA6 (GATA-Binding Protein 6)-Dependent and -Independent Vascular Smooth Muscle Cell Plasticity and Intimal HyperplasiaSrivastava R, Rolyan H, Xie Y, Li N, Bhat N, Hong L, Esteghamat F, Adeniran A, Geirsson A, Zhang J, Ge G, Nobrega M, Martin KA, Mani A. TCF7L2 (Transcription Factor 7-Like 2) Regulation of GATA6 (GATA-Binding Protein 6)-Dependent and -Independent Vascular Smooth Muscle Cell Plasticity and Intimal Hyperplasia Arteriosclerosis Thrombosis And Vascular Biology 2018, 39: 250-262. PMID: 30567484, PMCID: PMC6365015, DOI: 10.1161/atvbaha.118.311830.
- The interplay of canonical and noncanonical Wnt signaling in metabolic syndromeAbou Ziki M, Mani A. The interplay of canonical and noncanonical Wnt signaling in metabolic syndrome Progress In Food & Nutrition Science 2018, 70: 18-25. PMID: 30049588, PMCID: PMC6320319, DOI: 10.1016/j.nutres.2018.06.009.
- Abstract 618: Identification of Novel Disease Genes for Metabolic SyndromeMani A, Bhat N, Esteghamat S. Abstract 618: Identification of Novel Disease Genes for Metabolic Syndrome Arteriosclerosis Thrombosis And Vascular Biology 2018, 38 DOI: 10.1161/atvb.38.suppl_1.618.
- Addition of Estradiol to Cross-Sex Testosterone Therapy Reduces Atherosclerosis Plaque Formation in Female ApoE−/− MiceGoetz TG, Mamillapalli R, Sahin C, Majidi-Zolbin M, Ge G, Mani A, Taylor HS. Addition of Estradiol to Cross-Sex Testosterone Therapy Reduces Atherosclerosis Plaque Formation in Female ApoE−/− Mice Endocrinology 2017, 159: 754-762. PMID: 29253190, PMCID: PMC5774248, DOI: 10.1210/en.2017-00884.
- Endothelial APLNR regulates tissue fatty acid uptake and is essential for apelin’s glucose-lowering effectsHwangbo C, Wu J, Papangeli I, Adachi T, Sharma B, Park S, Zhao L, Ju H, Go GW, Cui G, Inayathullah M, Job JK, Rajadas J, Kwei SL, Li MO, Morrison AR, Quertermous T, Mani A, Red-Horse K, Chun HJ. Endothelial APLNR regulates tissue fatty acid uptake and is essential for apelin’s glucose-lowering effects Science Translational Medicine 2017, 9 PMID: 28904225, PMCID: PMC5703224, DOI: 10.1126/scitranslmed.aad4000.
- Deleterious protein‐altering mutations in the SCN10A voltage‐gated sodium channel gene are associated with prolonged QTZiki M, Seidelmann SB, Smith E, Atteya G, Jiang Y, Fernandes RG, Marieb MA, Akar JG, Mani A. Deleterious protein‐altering mutations in the SCN10A voltage‐gated sodium channel gene are associated with prolonged QT Clinical Genetics 2017, 93: 741-751. PMID: 28407228, PMCID: PMC5640462, DOI: 10.1111/cge.13036.
- Wnt signaling, a novel pathway regulating blood pressure? State of the art reviewZiki M, Mani A. Wnt signaling, a novel pathway regulating blood pressure? State of the art review Atherosclerosis 2017, 262: 171-178. PMID: 28522145, PMCID: PMC5508596, DOI: 10.1016/j.atherosclerosis.2017.05.001.
- DELETERIOUS MUTATIONS IN SCN10A ARE ASSOCIATED WITH LONG QT SYNDROMEZiki M, Seidelmann S, Smith E, Narayanan A, Atteya G, Jiang Y, Gil-Fernandez R, Marieb M, Akar J, Mani A. DELETERIOUS MUTATIONS IN SCN10A ARE ASSOCIATED WITH LONG QT SYNDROME Journal Of The American College Of Cardiology 2017, 69: 509. DOI: 10.1016/s0735-1097(17)33898-6.
- Application of Whole Exome Sequencing in the Clinical Diagnosis and Management of Inherited Cardiovascular Diseases in AdultsSeidelmann SB, Smith E, Subrahmanyan L, Dykas D, Abou Ziki MD, Azari B, Hannah-Shmouni F, Jiang Y, Akar JG, Marieb M, Jacoby D, Bale AE, Lifton RP, Mani A. Application of Whole Exome Sequencing in the Clinical Diagnosis and Management of Inherited Cardiovascular Diseases in Adults Circulation Genomic And Precision Medicine 2017, 10: e001573. PMID: 28087566, PMCID: PMC5245580, DOI: 10.1161/circgenetics.116.001573.
- Mutations in the Histone Modifier PRDM6 Are Associated with Isolated Nonsyndromic Patent Ductus ArteriosusLi N, Subrahmanyan L, Smith E, Yu X, Zaidi S, Choi M, Mane S, Nelson-Williams C, Behjati M, Kazemi M, Hashemi M, Fathzadeh M, Narayanan A, Tian L, Montazeri F, Mani M, Begleiter ML, Coon BG, Lynch HT, Olson EN, Zhao H, Ruland J, Lifton RP, Mani A. Mutations in the Histone Modifier PRDM6 Are Associated with Isolated Nonsyndromic Patent Ductus Arteriosus American Journal Of Human Genetics 2016, 99: 1000. PMID: 27716515, PMCID: PMC5065682, DOI: 10.1016/j.ajhg.2016.09.003.
- Mutations in the Histone Modifier PRDM6 Are Associated with Isolated Nonsyndromic Patent Ductus ArteriosusLi N, Subrahmanyan L, Smith E, Yu X, Zaidi S, Choi M, Mane S, Nelson-Williams C, Behjati M, Kazemi M, Hashemi M, Fathzadeh M, Narayanan A, Tian L, Montazeri F, Mani M, Begleiter ML, Coon BG, Lynch HT, Olson EN, Zhao H, Ruland J, Lifton RP, Mani A. Mutations in the Histone Modifier PRDM6 Are Associated with Isolated Nonsyndromic Patent Ductus Arteriosus American Journal Of Human Genetics 2016, 98: 1082-1091. PMID: 27181681, PMCID: PMC4908195, DOI: 10.1016/j.ajhg.2016.03.022.
- Metabolic syndromeZiki M, Mani A. Metabolic syndrome Current Opinion In Lipidology 2016, 27: 162-171. PMID: 26825138, PMCID: PMC5141383, DOI: 10.1097/mol.0000000000000276.
- IMPORTIN 4 ACTS AS A GENETIC MODIFIER OF LAMIN A/C ARG644CYS MUTATION IN PREDISPOITION FOR PREMATURE CORONARY ARTERY DISEASEZiki M, Smith E, Seidelmann S, Mani A. IMPORTIN 4 ACTS AS A GENETIC MODIFIER OF LAMIN A/C ARG644CYS MUTATION IN PREDISPOITION FOR PREMATURE CORONARY ARTERY DISEASE Journal Of The American College Of Cardiology 2016, 67: 589. DOI: 10.1016/s0735-1097(16)30590-3.
- CORONARY ARTERY DISSECTION IN EHLERS DANLOS SYNDROMESmith E, Mani A. CORONARY ARTERY DISSECTION IN EHLERS DANLOS SYNDROME Journal Of The American College Of Cardiology 2016, 67: 1018. DOI: 10.1016/s0735-1097(16)31019-1.
- Impaired LRP6-TCF7L2 Activity Enhances Smooth Muscle Cell Plasticity and Causes Coronary Artery DiseaseSrivastava R, Zhang J, Go GW, Narayanan A, Nottoli TP, Mani A. Impaired LRP6-TCF7L2 Activity Enhances Smooth Muscle Cell Plasticity and Causes Coronary Artery Disease Cell Reports 2015, 13: 746-759. PMID: 26489464, PMCID: PMC4626307, DOI: 10.1016/j.celrep.2015.09.028.
- The Protective Effect of Transcription Factor 7-Like 2 Risk Allele rs7903146 against Elevated Fasting Plasma Triglyceride in Type 2 Diabetes: A Meta-AnalysisWang S, Song K, Srivastava R, Fathzadeh M, Li N, Mani A. The Protective Effect of Transcription Factor 7-Like 2 Risk Allele rs7903146 against Elevated Fasting Plasma Triglyceride in Type 2 Diabetes: A Meta-Analysis Journal Of Diabetes Research 2015, 2015: 468627. PMID: 26576435, PMCID: PMC4631899, DOI: 10.1155/2015/468627.
- The Genetic Challenges and Opportunities in Advanced Heart FailureHannah-Shmouni F, Seidelmann SB, Sirrs S, Mani A, Jacoby D. The Genetic Challenges and Opportunities in Advanced Heart Failure Canadian Journal Of Cardiology 2015, 31: 1338-1350. PMID: 26518444, PMCID: PMC5423787, DOI: 10.1016/j.cjca.2015.07.735.
- DYRK1B modifies insulin action in liver and skeletal muscle and predispose to atherosclerosisFathzadeh M, Keramati A, Bazzaz J, Yarovinsky T, Sarajzadeh K, Amini M, Noorafshan A, Mehrabani D, Dianatpour M, Omrani G, Bigi M, Kasaei M, Poustchi H, Lifton R, Malekzadeh R, Mani A. DYRK1B modifies insulin action in liver and skeletal muscle and predispose to atherosclerosis Atherosclerosis 2015, 241: e23. DOI: 10.1016/j.atherosclerosis.2015.04.093.
- New targets to treat obesity and the metabolic syndromeMartin KA, Mani MV, Mani A. New targets to treat obesity and the metabolic syndrome European Journal Of Pharmacology 2015, 763: 64-74. PMID: 26001373, PMCID: PMC4573317, DOI: 10.1016/j.ejphar.2015.03.093.
- Abstract 20140: Minibrain Relate Kinase / Dyrk1B Links Skeletal Muscle Glycolytic Metabolism with Insulin Resistance and Causes Metabolic SyndromeFathzadeh M, Keramati A, Go G, Singh R, Sarajzadeh K, Tavakkoly-Bazzaz J, Noorafshan A, Kasaei M, Amini M, Omrani G, Babaee Bigi M, Babaei M, Hosseinian A, Malekzadeh R, Lifton R, Mani A. Abstract 20140: Minibrain Relate Kinase / Dyrk1B Links Skeletal Muscle Glycolytic Metabolism with Insulin Resistance and Causes Metabolic Syndrome Circulation 2014, 130 DOI: 10.1161/circ.130.suppl_2.20140.
- Wnt signaling, de novo lipogenesis, adipogenesis and ectopic fatSong K, Wang S, Mani M, Mani A. Wnt signaling, de novo lipogenesis, adipogenesis and ectopic fat Oncotarget 2014, 5: 11000-11003. PMID: 25526027, PMCID: PMC4294374, DOI: 10.18632/oncotarget.2769.
- The Metabolic Syndrome and DYRK1BKeramati AR, Fathzadeh M, Mani A. The Metabolic Syndrome and DYRK1B New England Journal Of Medicine 2014, 371: 784-786. PMID: 25140972, DOI: 10.1056/nejmc1408235.
- Plasma Cardiotrophin‐1 Levels are Associated With Hypertensive Heart Disease: A Meta‐AnalysisSong K, Wang S, Huang B, Luciano A, Srivastava R, Mani A. Plasma Cardiotrophin‐1 Levels are Associated With Hypertensive Heart Disease: A Meta‐Analysis Journal Of Clinical Hypertension 2014, 16: 686-692. PMID: 25052897, PMCID: PMC4159421, DOI: 10.1111/jch.12376.
- Syndromic Congenital Heart DiseasesMani A, Alizadehasl A. Syndromic Congenital Heart Diseases 2014, 65-69. DOI: 10.1007/978-1-4471-6383-1_10.
- The Combined Hyperlipidemia Caused by Impaired Wnt-LRP6 Signaling Is Reversed by Wnt3a RescueGo GW, Srivastava R, Hernandez-Ono A, Gang G, Smith SB, Booth CJ, Ginsberg HN, Mani A. The Combined Hyperlipidemia Caused by Impaired Wnt-LRP6 Signaling Is Reversed by Wnt3a Rescue Cell Metabolism 2014, 19: 209-220. PMID: 24506864, PMCID: PMC3920193, DOI: 10.1016/j.cmet.2013.11.023.
- Abstract 140: LRP6 Influences Body Fat and Glucose Homeostasis in Mouse by Activating mTOR Pathway and Inhibiting Mitochondrial Energy ExpenditureLiu W, Singh R, Choi C, Young L, Keramati A, Samuel V, Lifton R, Shulman G, Mani A. Abstract 140: LRP6 Influences Body Fat and Glucose Homeostasis in Mouse by Activating mTOR Pathway and Inhibiting Mitochondrial Energy Expenditure Arteriosclerosis Thrombosis And Vascular Biology 2012, 32 DOI: 10.1161/atvb.32.suppl_1.a140.
- Abstract 321: LRP6 Regulates LDL Receptor Internalization and LDL UptakeMani A, Go G, Ye Z, Singh R. Abstract 321: LRP6 Regulates LDL Receptor Internalization and LDL Uptake Arteriosclerosis Thrombosis And Vascular Biology 2012, 32 DOI: 10.1161/atvb.32.suppl_1.a321.
- Prevalence of Obesity and Traditional Cardiovascular Risk Factors in South AsiansKhanna P, Mani A. Prevalence of Obesity and Traditional Cardiovascular Risk Factors in South Asians Current Cardiovascular Risk Reports 2012, 6: 112-119. DOI: 10.1007/s12170-012-0220-x.
- Wild-type LRP6 inhibits, whereas atherosclerosis-linked LRP6R611C increases PDGF-dependent vascular smooth muscle cell proliferationKeramati AR, Singh R, Lin A, Faramarzi S, Ye ZJ, Mane S, Tellides G, Lifton RP, Mani A. Wild-type LRP6 inhibits, whereas atherosclerosis-linked LRP6R611C increases PDGF-dependent vascular smooth muscle cell proliferation Proceedings Of The National Academy Of Sciences Of The United States Of America 2011, 108: 1914-1918. PMID: 21245321, PMCID: PMC3033290, DOI: 10.1073/pnas.1019443108.
- W15 THE ANTIPROLIFERATIVE EFFECT OF LRP6 AND ITS IMPAIRMENT BY R611C MUTATION ARE MEDIATED BY INDEPENDENT INTERMEDIATES OF THE PDGF PATHWAYKeramati A, Singh R, Liu W, Faramarzi S, Nottoli T, Tellides G, Mani A. W15 THE ANTIPROLIFERATIVE EFFECT OF LRP6 AND ITS IMPAIRMENT BY R611C MUTATION ARE MEDIATED BY INDEPENDENT INTERMEDIATES OF THE PDGF PATHWAY Atherosclerosis Plus 2010, 11: 4. DOI: 10.1016/s1567-5688(10)70016-7.
- Bicuspid aortic valve: clinical approach and scientific review of a common clinical entityFriedman T, Mani A, Elefteriades JA. Bicuspid aortic valve: clinical approach and scientific review of a common clinical entity Expert Review Of Cardiovascular Therapy 2008, 6: 235-248. PMID: 18248277, DOI: 10.1586/14779072.6.2.235.
- The Aberrant Expression of Beta-catenin in Esophageal Squamous Cell Cancer (ESCC) in Northeastern IranMani S, Moradi A, Abdolahi N, Martel M, Semnani S, Glazer P, Mani A. The Aberrant Expression of Beta-catenin in Esophageal Squamous Cell Cancer (ESCC) in Northeastern Iran International Journal Of Radiation Oncology • Biology • Physics 2007, 69: s309-s310. DOI: 10.1016/j.ijrobp.2007.07.1366.
- In vivo cerulein hyperstimulation of rat pancreas is associated with redistribution of the cation-independent mannose 6-phoshate receptorKarne S, Mani A, Kolodecik T, Gorelick F, Haven C. In vivo cerulein hyperstimulation of rat pancreas is associated with redistribution of the cation-independent mannose 6-phoshate receptor Gastroenterology 2001, 120: a719. DOI: 10.1016/s0016-5085(08)83579-2.
- In vivo cerulein hyperstimulation of rat pancreas is associated with redistribution of the cation-independent mannose 6-phoshate receptorKARNE S, MANI A, KOLODECIK T, GORELICK F, CT H. In vivo cerulein hyperstimulation of rat pancreas is associated with redistribution of the cation-independent mannose 6-phoshate receptor Gastroenterology 2001, 120: a719-a719. DOI: 10.1016/s0016-5085(01)83579-4.
- Mechanism of desensitization of the cloned vasopressin V1a receptor expressed in Xenopus oocytesNathanson MH, Burgstahler AD, Orloff JJ, Mani A, Moyer MS. Mechanism of desensitization of the cloned vasopressin V1a receptor expressed in Xenopus oocytes American Journal Of Physiology 1994, 267: c94-c103. PMID: 8048495, DOI: 10.1152/ajpcell.1994.267.1.c94.