Email

u245824@bcm.edu

Positions

Postdoctoral Associate

Center for Precision Environmental Health
Baylor College of Medicine

Addresses

One Baylor Plaza (Lab)

Houston
United States

Education

PhD from Ludwig Maximilian University of Munich

08/2021 - Munich, Baveria Germany

MSc from University of Hyderabad

04/2015 - Hyderabad, Telangana India

BSc from Andhra University

05/2013 - Bhimavaram, Andhra Pradesh India

Professional Statement

I was trained as a renal biochemist during my graduate training and as a biochemist during my master’s. So, I have a wide variety of training and experience in basic research, including cell biology and translational research, such as renal cancer chemoprevention/chemoprotection. I lead various projects such as delaying the progression of chronic kidney diseases, Mechanism of crystals formation in the kidney and inhibition of kidney crystals formation and immune cell activation during obesity-induced diabetic conditions, and the role of cilia in polycystic kidney diseases. During my postdoctoral training, I was part of an exciting discovery that the primary cilia are mechanical sensors for cyst growth in polycystic kidney diseases. Recently, our group identified methyltransferase SETD2, responsible for H3 lysine 36 trimethylation (H3K36me3) of chromatin and methylate microtubules (Cell 2016). Since primary cilia is a microtubule structure, identifying “readers” for the SETD2 methyl mark on microtubules can fill critical knowledge gaps in our understanding of how defects in chromatin remodelers influence the cilia, such as formation retraction and instability. In my current project, I am focusing on ‘cilia’ and hypothesize that chromatin remodeler SETD2 and KDM4A recognize this methylation and acetylation marks could influence the cilia. I have extensive laboratory experience, including Western blotting, Cell culture, gene cloning, site-directed mutagenesis, genetic and inducible knockout models including flox-ER-care and knockdown using lentiviral shRNA, CRISPR, immunocytochemistry including visualizing the primary cilia, live-cell imaging and protein-protein interactions (immunoprecipitation, peptide pull-downs), cell phenotyping (proliferation, cell cycle/synchronization). In addition, I also played a technical director role in my lab and trained several rotation graduates and medical students. I have collaborated with many researchers and contributed to the peer-reviewed literature from each project.

Videos

Selected Publications

• "Drug Testing for Residual Progression of Diabetic Kidney Disease in Mice Beyond Therapy with Metformin, Ramipril, and Empagliflozin." JASN. 2020 Aug; Pubmed PMID: 32576600
• "Epigenomic and transcriptional profiling identifies impaired glyoxylate detoxification in NAFLD as a risk factor for hyperoxaluria." Cell Reports.;
• "Growth hormone induces mitotic catastrophe of glomerular podocytes and contributes to proteinuria." Cell Death Disease.; Pubmed PMID: 33795655
• "Inhibitors of Calcium Oxalate Crystallization for the Treatment of Oxalate Nephropathies." Advanced Science.; Pubmed PMID: 32328427

Projects

Drug Testing for Residual Progression of Diabetic Kidney Disease in Mice Beyond Therapy with Metformin, Ramipril, and Empagliflozin

Ludwig Maximilian University of Munich (08/2017 - 08/2021)

Munich

Progression of CKD in type 2 diabetes, despite dual inhibition of sodium-glucose transporter-2 and the renin-angiotensin system, remains a concern. Bromoindirubin-3'-oxime (BIO), previously reported to promote podocyte survival and regeneration, is a candidate additional drug to elicit renoprotective effects beyond therapy with metformin, ramipril, and empagliflozin (MRE). Evaluating a drug with standard therapeutics more closely mimics the clinical setting than evaluating the drug alone. Add-on treatment with BIO for only 4 weeks attenuates progression of CKD beyond MRE therapy in mice with type 2 diabetes. Additional drug combinations may help to further delay ESKD in type 2 diabetes.

Define the Sensor and Effectors of Synchronous (Physiologic) and Asynchronous (PKD) GTS.

Yale University (09/2021 - 09/2022)

New Haven

Analysis of the physiologic tubular response to hyperfiltration reveals that cell proliferation and tubule remodeling occur rapidly and synchronously following an acute increase in GFR. Throughout this adaptive response, each individual tubule enlarges both radially and longitudinally while maintaining a precise morphology with a proportional increase in the epithelial, brush border and lumen areas relative to the total tubular area. In contrast, tubules that lack Pc1 spontaneously undergo asynchronous radial expansion that is markedly exaggerated (i.e. cystic dilation) following an acute increase in filtration.

Role of chromatin modifiers at Primary Cilia

Baylor College of Medicine (09/2022 - present)

Houston

Languages

Telugu, Hindi, German