A5016580341- Cell death mechanisms and regulation
- Mitochondrial Function and Pathology
- RNA Interference and Gene Delivery
- Epigenetics and DNA Methylation
- Cancer-related Molecular Pathways
- ATP Synthase and ATPases Research
- Cancer, Hypoxia, and Metabolism
- Immune Cell Function and Interaction
- Phagocytosis and Immune Regulation
- Autophagy in Disease and Therapy
- Cancer Research and Treatments
- Melanoma and MAPK Pathways
- Immunotherapy and Immune Responses
- interferon and immune responses
- Ubiquitin and proteasome pathways
- RNA modifications and cancer
- Cell Image Analysis Techniques
- Histone Deacetylase Inhibitors Research
- Synthesis and Catalytic Reactions
- T-cell and B-cell Immunology
- Sphingolipid Metabolism and Signaling
- Pancreatic function and diabetes
- Metabolism and Genetic Disorders
- Mast cells and histamine
- Advanced biosensing and bioanalysis techniques
Icahn School of Medicine at Mount Sinai
2016-2025
Tisch Hospital
2013-2024
Tisch Cancer Institute
2011-2024
The Graduate Center, CUNY
2013-2024
New York Proton Center
2013-2023
Cancer Institute (WIA)
2013-2022
University of South Florida
2014
Angiologica (Italy)
2014
Sadick Dermatology
2014
St. Jude Children's Research Hospital
2006-2013
The tumor suppressor p53 exerts its anti-neoplastic activity primarily through the induction of apoptosis. We found that cytosolic localization endogenous wild-type or trans-activation-deficient was necessary and sufficient for directly activated proapoptotic Bcl-2 protein Bax in absence other proteins to permeabilize mitochondria engage apoptotic program. also released both multidomain BH3-only [Proapoptotic family share only third homology domain (BH3)] were sequestered by Bcl-xL....
The Trp53 tumor suppressor gene product (p53) functions in the nucleus to regulate proapoptotic genes, whereas cytoplasmic p53 directly activates Bcl-2 proteins permeabilize mitochondria and initiate apoptosis. Here, we demonstrate that a tripartite nexus between Bcl-xL, p53, PUMA coordinates these distinct functions. After genotoxic stress, Bcl-xL sequestered p53. Nuclear caused expression of PUMA, which then displaced from allowing induce mitochondrial permeabilization. Mutant bound but...
While scientific environments have been described as unwelcoming to the LGBGQ+ community, and fields like physics systematically documented these challenges, climate in biology workplaces has not assessed. We conducted largest survey date of LGBTQ+ experiences biology, including 1419 biologists across five professional societies, with 486 identifying LGBTQ+. Trans gender non-conforming (TGNC) reported lower belonging morale within workplace, community compared cis, straight biologists. They...
The mitochondrial pathway of apoptosis in vertebrates is dependent on the process outer membrane permeabilization (MOMP), which leads to release proteins from intermembrane space into cytosol. "Upstairs" this event are Bcl-2 family that regulate and mediate MOMP; "downstairs" activation caspases orchestrate dismantling cell. In Connections Map database at Science's Signal Transduction Knowledge Environment (STKE), pathways define apotosis illustrated, with bulk control occurring "upstairs" MOMP.
Normal cellular lifespan is contingent upon preserving outer mitochondrial membrane (OMM) integrity, as permeabilization promotes apoptosis. BCL-2 family proteins control (MOMP) by regulating the activation of pro-apoptotic effector molecules, BAX and BAK. Sustainable stress induces (e.g., BID, BIM, cytosolic p53) capable directly activating and/or BAK, but these direct activators are sequestered anti-apoptotic BCL-2, BCL-xL, MCL-1). In event accumulated or marked stress, a coordinated...