Projects per year
Personal profile
Area of Expertise
My laboratory is interested in understanding the pathological mechanisms involved in glaucomatous damage to trabecular meshwork (TM) and retinal ganglion cells (RGCs). Our primary focus is to understand the role of protein misfolding and its associated cellular processes including endoplasmic reticulum (ER) stress and autophagy in the glaucomatous TM damage.
We have developed two novel glaucoma mouse models and have established various genetic tools to study protein misfolding and biological functions of unfolded protein response pathway and autophagy in glaucoma pathogenesis. We are currently pursuing gene therapy via CRISPR genome editing and small chemicals to develop targeted treatment for primary open angle glaucoma.
We have developed two novel glaucoma mouse models and have established various genetic tools to study protein misfolding and biological functions of unfolded protein response pathway and autophagy in glaucoma pathogenesis. We are currently pursuing gene therapy via CRISPR genome editing and small chemicals to develop targeted treatment for primary open angle glaucoma.
Education/Academic qualification
PhD in Cell Biology & Genetics, UNT Health Science Center
Fingerprint
Dive into the research topics where Gulab Zode is active. These topic labels come from the works of this person. Together they form a unique fingerprint.
- 1 Similar Profiles
Network
Recent external collaboration on country/territory level. Dive into details by clicking on the dots or
-
Novel Genome Editing for the Treatment of Glaucoma
Clark, A., Zode, G. & SHEFFIELD, V.
1/07/19 → 30/04/22
Project: Research
-
Novel Genome Editing for the Treatment of Glaucoma
Clark, A., Zode, G. & SHEFFIELD, V.
1/07/19 → 30/04/22
Project: Research
-
Targeting ER Stress Pathway Using Sodium 4-Phenylbutyrate for the Treatment of POAG
Zode, G. & ZODE, G.
30/09/18 → 30/06/22
Project: Research
-
Targeting ER Stress Pathway using Sodium 4-phenylbutyrate for the Treatment of POAG
30/09/18 → 30/06/22
Project: Research
-
-
Autophagy stimulation reduces ocular hypertension in a murine glaucoma model via autophagic degradation of mutant myocilin
Kasetti, R. B., Maddineni, P., Kiehlbauch, C., Patil, S., Searby, C. C., Levine, B., Sheffield, V. C. & Zode, G. S., 8 Mar 2021, In: JCI Insight. 6, 5, e143359.Research output: Contribution to journal › Article › peer-review
Open Access1 Scopus citations -
Caveolar peroxynitrite formation impairs endothelial TRPV4 channels and elevates pulmonary arterial pressure in pulmonary hypertension
Daneva, Z., Marziano, C., Ottolini, M., Chen, Y. L., Baker, T. M., Kuppusamy, M., Zhang, A., Ta, H. Q., Reagan, C. E., Mihalek, A. D., Kasetti, R. B., Shen, Y., Isakson, B. E., Minshall, R. D., Zode, G. S., Goncharova, E. A., Laubach, V. E. & Sonkusare, S. K., 27 Apr 2021, In: Proceedings of the National Academy of Sciences of the United States of America. 118, 17, e2023130118.Research output: Contribution to journal › Article › peer-review
-
Impaired TRPV4-eNOS signaling in trabecular meshwork elevates intraocular pressure in glaucoma
Patel, P. D., Chen, Y. L., Kasetti, R. B., Maddineni, P., Mayhew, W., Millar, J. C., Ellis, D. Z., Sonkusare, S. K. & Zode, G. S., 20 Apr 2021, In: Proceedings of the National Academy of Sciences of the United States of America. 118, 16, e2022461118.Research output: Contribution to journal › Article › peer-review
Open Access -
Sodium 4-phenylbutyrate reduces ocular hypertension by degrading extracellular matrix deposition via activation of MMP9
Maddineni, P., Kasetti, R. B., Kodati, B., Yacoub, S. & Zode, G. S., Sep 2021, In: International journal of molecular sciences. 22, 18, 10095.Research output: Contribution to journal › Article › peer-review
Open Access -
ATF4 leads to glaucoma by promoting protein synthesis and ER client protein load
Kasetti, R. B., Patel, P. D., Maddineni, P., Patil, S., Kiehlbauch, C., Millar, J. C., Searby, C. C., Raghunathan, V. K., Sheffield, V. C. & Zode, G. S., 1 Dec 2020, In: Nature Communications. 11, 1, 5594.Research output: Contribution to journal › Article › peer-review
Open Access4 Scopus citations