B I O G R A P H Y
Ph.D. - Borkovich Lab, University of California, Riverside
Former Post Doctoral Fellow - Bennett Lab, University of California, San Diego
Former Post Doctoral Researcher - Fowler Lab, University of Delaware, Newark
Associate Scientist, UD Flow Cytometry Core Manager, University of Delaware, Newark
Former Post Doctoral Fellow - Bennett Lab, University of California, San Diego
Former Post Doctoral Researcher - Fowler Lab, University of Delaware, Newark
Associate Scientist, UD Flow Cytometry Core Manager, University of Delaware, Newark
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Current Research - UD Flow Cytometry Core (U of Delaware) -
Heme biogenesis and Erythroid differentiation regulation by proteasomal and translational machineries
-In development -
Post-doctoral Research - Fowler Lab (U of Delaware) - Cytoskeletal dynamics during erythroid differentiation
In the Fowler lab, I have been interested in the role of actin reorganization during erythroid differentiation. The major focus in the lab is to understand how actin is reorganized during early and terminal erythroid differentiation (ED). Specific to the lab - I have also brought in renewed focus on what roles upstream signaling processes play during ED and how this might relate to actin filament formation. How would the actin machinery coordinate erythroid differentiation in conjunction with apoptotic machineries or other signaling mechanisms? Using ideas, concepts and tools I have learnt from my previous research endeavors I am looking to understand these intricate cell biological processes in a new light. Overall I aspire to culminate these experiences into an independent research group in the near future.
Post-doctoral Research - Bennett Lab (UC San Diego) - E3 ligase biology and ribosomal quality control
Here my research focused on how proteostasis mechanisms are regulated via ribosomal machineries; ribosomal quality control (RQC) coupled to ubiquitination of nascent proteins as well what non-RQC functions might the E3 ligases regulate. Broadly speaking we looked into mapping interactions in the mammalian ribosomal landscape and how E3 ligases and various components of the UPS (ubiquitin proteasome system) regulate functionalities during proteostasis. Implications of these processes impinge on important cellular pathways critical to cancer progression, neuro-degeneration and similar disease pathogenesis.
Ph.D. studies - Borkovich Lab (UC Riverside) - G protein signaling, amino acid starvation and signal transduction
My studies focused on understanding the molecular machineries behind regulation of various aspects of fungal biology using Neurospora crassa as a model system. One such aspect was the importance of protein phosphatases in fungal cells and how deletion of these important genes leads to developmental defects in fungi. We have also demonstrated that these phosphatases are crucial for regulating the p38 mitogen-activated kinase and deletion of certain protein phosphatases can lead to mis-regulation and increased phosphorylation of the p38 MAPK possibly leading to developmental defects. Additionally, I also studied the nature of amino acid starvation/general amino acid control (GAAC or known as integrated stress response, ISR in mammals) on fungal biology as we aimed to unravel certain unanswered questions with regards to general amino acid control in fungi. One important hub for general amino acid control in fungi is the WD40 protein and RACK1 homolog - CPC-2 and has been the focus of our studies. I have also been interested in the function of GPCRs and G proteins in amino acid starvation and looking at GPCRs as a critical component of GAAC/ISR. Some aspects of this work might also be followed through by me in the future.
Current Research - UD Flow Cytometry Core (U of Delaware) -
Heme biogenesis and Erythroid differentiation regulation by proteasomal and translational machineries
-In development -
Post-doctoral Research - Fowler Lab (U of Delaware) - Cytoskeletal dynamics during erythroid differentiation
In the Fowler lab, I have been interested in the role of actin reorganization during erythroid differentiation. The major focus in the lab is to understand how actin is reorganized during early and terminal erythroid differentiation (ED). Specific to the lab - I have also brought in renewed focus on what roles upstream signaling processes play during ED and how this might relate to actin filament formation. How would the actin machinery coordinate erythroid differentiation in conjunction with apoptotic machineries or other signaling mechanisms? Using ideas, concepts and tools I have learnt from my previous research endeavors I am looking to understand these intricate cell biological processes in a new light. Overall I aspire to culminate these experiences into an independent research group in the near future.
Post-doctoral Research - Bennett Lab (UC San Diego) - E3 ligase biology and ribosomal quality control
Here my research focused on how proteostasis mechanisms are regulated via ribosomal machineries; ribosomal quality control (RQC) coupled to ubiquitination of nascent proteins as well what non-RQC functions might the E3 ligases regulate. Broadly speaking we looked into mapping interactions in the mammalian ribosomal landscape and how E3 ligases and various components of the UPS (ubiquitin proteasome system) regulate functionalities during proteostasis. Implications of these processes impinge on important cellular pathways critical to cancer progression, neuro-degeneration and similar disease pathogenesis.
Ph.D. studies - Borkovich Lab (UC Riverside) - G protein signaling, amino acid starvation and signal transduction
My studies focused on understanding the molecular machineries behind regulation of various aspects of fungal biology using Neurospora crassa as a model system. One such aspect was the importance of protein phosphatases in fungal cells and how deletion of these important genes leads to developmental defects in fungi. We have also demonstrated that these phosphatases are crucial for regulating the p38 mitogen-activated kinase and deletion of certain protein phosphatases can lead to mis-regulation and increased phosphorylation of the p38 MAPK possibly leading to developmental defects. Additionally, I also studied the nature of amino acid starvation/general amino acid control (GAAC or known as integrated stress response, ISR in mammals) on fungal biology as we aimed to unravel certain unanswered questions with regards to general amino acid control in fungi. One important hub for general amino acid control in fungi is the WD40 protein and RACK1 homolog - CPC-2 and has been the focus of our studies. I have also been interested in the function of GPCRs and G proteins in amino acid starvation and looking at GPCRs as a critical component of GAAC/ISR. Some aspects of this work might also be followed through by me in the future.