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Nahid F. Mivechi

Researcher at Georgia Regents University

Publications -  55
Citations -  2927

Nahid F. Mivechi is an academic researcher from Georgia Regents University. The author has contributed to research in topics: Heat shock protein & Heat shock factor. The author has an hindex of 28, co-authored 53 publications receiving 2657 citations. Previous affiliations of Nahid F. Mivechi include Charlie Norwood VA Medical Center.

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Glycogen Synthase Kinase 3β and Extracellular Signal-Regulated Kinase Inactivate Heat Shock Transcription Factor 1 by Facilitating the Disappearance of Transcriptionally Active Granules after Heat Shock

TL;DR: It is demonstrated that newly synthesized pre-mRNAs colocalize to the HSF-1 punctate granules after heat shock, suggesting that these granules are sites of transcription, and evidence that glycogen synthase kinase 3β (GSK-3β) and extracellular signal-regulated kinase mitogen-activated protein kinase (ERK MAPK) participate in the down regulation of HSF -1 transcriptional activity.
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Targeted disruption of hsf1 leads to lack of thermotolerance and defines tissue-specific regulation for stress-inducible Hsp molecular chaperones.

TL;DR: It is demonstrated that Hsf1 is critical for maintaining cellular integrity after heat stress and that cells from hsf1−/− mice lack the ability to develop thermotolerance.
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Targeted disruption of the heat shock transcription factor (hsf)-2 gene results in increased embryonic lethality, neuronal defects, and reduced spermatogenesis.

TL;DR: It is reported here that hsf2−/− mice exhibit multiple phenotypes, including an increased prenatal lethality occurring between mid‐gestation to birth, with fetal death probably due to central nervous system defects including collapse of the lateral ventricles and ventricular hemorrhages, and suggest that hSF2 has a major function in controlling expression of genes important for embryonic development and maintenance of sperm production.
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Selective suppression of lymphomas by functional loss of Hsf1 in a p53-deficient mouse model for spontaneous tumors

TL;DR: The data presented here link the loss of Hsf1-dependent function to decreased susceptibility to spontaneous lymphomagenesis, which may have implications for cancer prevention and therapy.
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Insights into Regulation and Function of the Major Stress-Induced hsp70 Molecular Chaperone In Vivo: Analysis of Mice with Targeted Gene Disruption of the hsp70.1 or hsp70.3 Gene

TL;DR: It is reported here that the expression of hsp70.1 andhsp 70.3 is developmentally regulated at the transcriptional level, and an overlapping expression pattern for both genes is observed during embryo development and in the tissues of adult mice.