Z
Zahra Bahrami-Nejad
Researcher at Stanford University
Publications - 14
Citations - 173
Zahra Bahrami-Nejad is an academic researcher from Stanford University. The author has contributed to research in topics: Adipogenesis & Progenitor cell. The author has an hindex of 4, co-authored 13 publications receiving 118 citations.
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Journal ArticleDOI
A Transcriptional Circuit Filters Oscillating Circadian Hormonal Inputs to Regulate Fat Cell Differentiation.
Zahra Bahrami-Nejad,Minglei Zhao,Stefan Tholen,Devon M. Hunerdosse,Karen E. Tkach,Sabine N. S. van Schie,Mingyu Chung,Mary N. Teruel +7 more
TL;DR: The mechanism of how hormone oscillations are filtered as a combination of slow and fast positive feedback centered on PPARG is identified, providing a molecular mechanism for why stress, Cushing's disease, and other conditions for which glucocorticoid secretion loses its pulsatility may lead to obesity.
Journal ArticleDOI
Comparative genetic screens in human cells reveal new regulatory mechanisms in WNT signaling.
Andres M. Lebensohn,Ramin Dubey,Leif R. Neitzel,Ofelia Tacchelly-Benites,Eungi Yang,Caleb D. Marceau,Eric M. Davis,Bhaven B. Patel,Zahra Bahrami-Nejad,Kyle J. Travaglini,Yashi Ahmed,Ethan Lee,Jan E. Carette,Rajat Rohatgi +13 more
TL;DR: A systematic forward genetic analysis through reporter-based screens in haploid human cells uncovered new regulatory features at most levels of canonical WNT signaling that should enable the comprehensive understanding of other signaling systems.
Journal ArticleDOI
Chromatin-Remodeling Complex SWI/SNF Controls Multidrug Resistance by Transcriptionally Regulating the Drug Efflux Pump ABCB1.
Ramin Dubey,Andres M. Lebensohn,Zahra Bahrami-Nejad,Caleb D. Marceau,Magali Champion,Olivier Gevaert,Branimir I. Sikic,Jan E. Carette,Rajat Rohatgi +8 more
TL;DR: It is proposed that residual SWI/SNF complexes lacking SMARCB1 are vital determinants of drug sensitivity, not just to TOP2A-targeted agents, but to the much broader range of cancer drugs effluxed by ABCB1.
Journal ArticleDOI
Molecular Competition in G1 Controls When Cells Simultaneously Commit to Terminally Differentiate and Exit the Cell Cycle.
Michael L Zhao,Atefeh Rabiee,Kyle M. Kovary,Zahra Bahrami-Nejad,Brooks Taylor,Mary N. Teruel,Mary N. Teruel +6 more
TL;DR: Using live, single-cell imaging of cell cycle progression and differentiation commitment during adipogenesis, it is shown that a rapid switch mechanism engages exclusively in G1 to trigger differentiation commitment simultaneously with permanent exit from the cell cycle.
Posted ContentDOI
Molecular competition in G1 controls when cells simultaneously commit to terminally differentiate and exit the cell-cycle
Michael L Zhao,Atefeh Rabiee,Kyle M. Kovary,Zahra Bahrami-Nejad,Brooks Taylor,Mary N. Teruel +5 more
TL;DR: A rapid switch mechanism engages exclusively in G1 to trigger a simultaneous commitment to differentiate and permanently exit from the cell cycle and the differentiation control system is able to couple mitogen and differentiation stimuli to sustain a long-term balance between terminally differentiating cells and maintaining the progenitor cell pool.