Sravan Perla, PhD, MSc
Associate Research Scientist in PharmacologyCards
About
Research
Publications
2024
Mitogen-Activated Protein Kinase Phosphatase-5 is Required for TGF-β Signaling Through a JNK-Dependent Pathway.
Dorry S, Perla S, Bennett AM. Mitogen-Activated Protein Kinase Phosphatase-5 is Required for TGF-β Signaling Through a JNK-Dependent Pathway. Mol Cell Biol 2024, 1-15. PMID: 39607740, DOI: 10.1080/10985549.2024.2426665.Peer-Reviewed Original ResearchMitogen-Activated Protein Kinase Phosphatase-5 is Required for TGF-β Signaling Through a JNK-Dependent Pathway
Dorry S, Perla S, Bennett A. Mitogen-Activated Protein Kinase Phosphatase-5 is Required for TGF-β Signaling Through a JNK-Dependent Pathway. Molecular And Cellular Biology 2024, ahead-of-print: 1-15. PMID: 39607740, DOI: 10.1080/10985549.2024.2426665.Peer-Reviewed Original ResearchMitogen-activated protein kinaseTGF-b signalingMKP-5JNK-dependent pathwayFamily of protein phosphatasesNon-canonical sitesJNK-dependent mannerP38 mitogen-activated protein kinaseMitogen-activated protein kinase phosphatase-5JNK-dependentTranscriptional activityProtein phosphatasesTranscriptome analysisRNA sequencingProtein kinaseJNK inactivationNuclear translocationSignaling activityTGF-bSmad2 phosphorylationPharmacological inhibitionDrivers of fibrosisTissue fibrosisFactor BPathwayMAPK Phosphatase-5 is required for TGF-β signaling through a JNK-dependent pathway
Samuel J Dorry, Sravan Perla, Anton M Bennett bioRxiv 2024.06.27.600976; doi: https://doi.org/10.1101/2024.06.27.600976Peer-Reviewed Original ResearchAntiseizure Medications in Post-stroke Seizures: A Systematic Review and Network Meta-analysis (P8-1.012)
Misra S, Dawson J, Kwan P, Kasner S, Grotta J, Larsson D, Tanaka T, Zaveri H, Wang S, Khan E, Funaro M, Perla S, Dev P, Hussain T, Liebeskind D, Yasuda C, Elshahat A, Hitawala G, Wang E, Kitagawa R, Pathak A, Zhao Y, Scalzo F, Ihara M, Zelano J, Sunnerhagen K, Walters M, Jette N, Quinn T, Mishra N. Antiseizure Medications in Post-stroke Seizures: A Systematic Review and Network Meta-analysis (P8-1.012). Neurology 2024, 102 DOI: 10.1212/wnl.0000000000205632.Peer-Reviewed Original Research
2023
Identification of Protein Tyrosine Phosphatase (PTP) Substrates
Perla S, Qiu B, Dorry S, Yi J, Bennett A. Identification of Protein Tyrosine Phosphatase (PTP) Substrates. Methods In Molecular Biology 2023, 2743: 123-133. PMID: 38147212, DOI: 10.1007/978-1-0716-3569-8_8.Peer-Reviewed Original ResearchEpigenetic and transcriptional regulation of the human angiotensinogen gene by high salt
Perla S, Kumar A. Epigenetic and transcriptional regulation of the human angiotensinogen gene by high salt. BioRxiv 2023 PMID: 38045346, DOI: 10.1101/2023.11.22.568343.Peer-Reviewed Original Research
2022
An Assessment of the Therapeutic Landscape for the Treatment of Heart Disease in the RASopathies
Yi JS, Perla S, Bennett AM. An Assessment of the Therapeutic Landscape for the Treatment of Heart Disease in the RASopathies. Cardiovascular Drugs And Therapy 2022, 37: 1193-1204. PMID: 35156148, DOI: 10.1007/s10557-022-07324-0.Peer-Reviewed Original ResearchConceptsRAS-MAPK pathwayRAS/mitogen-activated protein kinase (MAPK) pathwayMitogen-activated protein kinase pathwayPost-developmental processesProtein kinase pathwayHypertrophic cardiomyopathyKinase pathwayRASopathy patientsDevelopmental diseasesNoonan syndromeTreatment of HCMRASopathiesCardiofaciocutaneous syndromePathwayNeurofibromatosis type 1Cardiovascular defectsValvular abnormalitiesCardiovascular manifestationsHeart diseaseClinical informationCostello syndromeCongenital heartMultiple lentiginesTherapeutic landscapeAntineoplastic drugs
2021
Low-dose Dasatinib Ameliorates Hypertrophic Cardiomyopathy in Noonan Syndrome with Multiple Lentigines
Yi JS, Perla S, Huang Y, Mizuno K, Giordano FJ, Vinks AA, Bennett AM. Low-dose Dasatinib Ameliorates Hypertrophic Cardiomyopathy in Noonan Syndrome with Multiple Lentigines. Cardiovascular Drugs And Therapy 2021, 36: 589-604. PMID: 33689087, PMCID: PMC9270274, DOI: 10.1007/s10557-021-07169-z.Peer-Reviewed Original ResearchConceptsHypertrophic cardiomyopathyNSML miceDasatinib treatmentLow-dose dasatinib treatmentPK propertiesMultiple lentiginesHeart tissueDasatinib-treated miceExposure-dependent inhibitionSrc homology 2 domain-containing protein tyrosine phosphatase 2Development of HCMAssessment of markersAutosomal dominant disorderNSML patientsDasatinib administrationCardiac fibrosisEffective target engagementEffective therapyConclusionThese dataMouse modelPharmacodynamic propertiesPK parametersHCM progressionDasatinibNoonan syndrome
2020
Tyrosyl phosphorylation of PZR promotes hypertrophic cardiomyopathy in PTPN11-associated Noonan syndrome with multiple lentigines
Yi JS, Perla S, Enyenihi L, Bennett AM. Tyrosyl phosphorylation of PZR promotes hypertrophic cardiomyopathy in PTPN11-associated Noonan syndrome with multiple lentigines. JCI Insight 2020, 5 PMID: 32584792, PMCID: PMC7455087, DOI: 10.1172/jci.insight.137753.Peer-Reviewed Original ResearchConceptsProtein tyrosine phosphataseTyrosyl phosphorylationNSML micePhosphorylation-defective mutantPTPN11 mutationsS6 kinase activityPZR tyrosyl phosphorylationTyrosine phosphataseS6 kinasePathophysiological signalingKinase activityShp2 interactionMutant fibroblastsSHP2Transmembrane glycoproteinMultiple lentiginesNoonan syndromeCraniofacial defectsPTPN11 geneHeart lysatesPhosphorylationSHP2 bindingMutationsNF-κB pathwayProtein zero
2019
A polymorphism in intron I of the human angiotensinogen gene (hAGT) affects binding by HNF3 and hAGT expression and increases blood pressure in mice
Mopidevi B, Kaw MK, Sivankutty I, Jain S, Perla SK, Kumar A. A polymorphism in intron I of the human angiotensinogen gene (hAGT) affects binding by HNF3 and hAGT expression and increases blood pressure in mice. Journal Of Biological Chemistry 2019, 294: 11829-11839. PMID: 31201268, PMCID: PMC6682742, DOI: 10.1074/jbc.ra119.007715.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensinogenAnimalsBinding SitesBlood PressureCCAAT-Enhancer-Binding Protein-betaChromatinHep G2 CellsHepatocyte Nuclear Factor 3-betaHumansIntronsLinkage DisequilibriumLiverMiceMice, Inbred C57BLMice, TransgenicPolymorphism, Single NucleotideProtein BindingReceptors, GlucocorticoidReninRNA, MessengerConceptsIntron IHap-IITransgenic animalsGenome-wide association studiesHepatocyte nuclear factor 3Reporter gene constructsBlood pressureCCAAT enhancer-binding protein βEnhancer-binding protein βHuman angiotensinogen geneStrong homologyHypoxanthine-guanine phosphoribosyltransferase locusNucleotide sequenceGene constructsTranscription rateHuman renin genePromoter activityAssociation studiesHAGT expressionMain haplotypesGenesProtein βElevated blood pressureTransgenic mouse modelFactor 3