Prohibitin and the senescent phenotype

@article{Dellorco1996ProhibitinAT,
  title={Prohibitin and the senescent phenotype},
  author={Robert T. Dell'orco and J. Keith McClung and Eldon Ralph Jupe and X-T. Liu},
  journal={Experimental Gerontology},
  year={1996},
  volume={31},
  pages={245-252}
}
Identification and Analysis of Prohibitin in B16 Mouse Melanoma Cells
TLDR
This work validated the initial findings reported using this cell line and 2D gel electrophoresis, as well as attempt to identify, isolate, and analyze prohibitin using mass spectrometry in order to determine if in its function within the cell, prohibitin was in any way being modified.
Capstones 1-1-2008 Identification and Analysis of Prohibitin in B 16 Mouse Melanoma Cells
TLDR
This work validated the initial findings reported using this cell line and 2D gel electrophoresis, as well as attempt to identify, isolate, and analyze prohibitin using mass spectrometry in order to determine if in its function within the cell, prohibitin was in any way being modified.
Prohibitin physically interacts with MCM proteins and inhibits mammalian DNA replication
TLDR
It is demonstrated that prohibitin can function as a potent inhibitor of DNA replication by interacting with members of Minichromosome maintenance complex of proteins (MCM2-7) and this might contribute to the growth regulatory properties of prohibitin.
Prohibitin Facilitates Cellular Senescence by Recruiting Specific Corepressors To Inhibit E2F Target Genes
TLDR
It is shown that senescence induced by DNA-damaging agents causes the localization of prohibitin to specific heterochromatic foci, and that prohibitin plays a vital role in inducing cellularsenescence.
Involvement of Prohibitin Upregulation in Abrin-Triggered Apoptosis
TLDR
The data show that prohibitin (PHB), a tumor suppressor protein, is significantly upregulated in ABR-triggered apoptosis and nuclear translocation of the PHB-p53 complex may play a role in the transcription of Bax.
Prohibitin is a cholesterol‐sensitive regulator of cell cycle transit
TLDR
It is demonstrated using unbiased proteomics and standard biochemistry that cholesterol insufficiency causes upregulation of prohibitin, an inhibitor of cell cycle progression, through activation of a cholesterol‐responsive promoter element.
Hyperphosphorylation of a Mitochondrial Protein, Prohibitin, Is Induced by Calyculin A in a Rice Lesion-Mimic Mutant cdr11
TLDR
Analysis of green fluorescent protein fusions indicated that rice PHB (OsPHB1) was targeted to mitochondria as found in yeast and mammals, suggesting a possibility that PHB is involved in defense response and/or programmed cell death through the mitochondrial function.
Apoptosis of rat granulosa cells after staurosporine and serum withdrawal is suppressed by adenovirus-directed overexpression of prohibitin.
TLDR
Evidence is provided that prohibitin could serve an antiapoptotic role in undifferentiated granulosa cells by markedly attenuating the ability of STS and serum withdrawal to induce apoptosis via the intrinsic apoptotic pathway.
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References

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Prohibitin expression during cellular senescence of human diploid fibroblasts.
TLDR
Results suggest that prohibitin is similar to the retinoblastoma gene product whose anti-proliferative activity remains active in older cells because it is not post-synthetically modified.
Prohibitin antiproliferative activity and lack of heterozygosity in immortalized cell lines.
TLDR
Results suggest that prohibitin may play a role as a tumor suppressor in the immortalization of Group B cells, and using Southern and single-strand conformation polymorphism analyses distinguished two alleles.
Prohibitin, an evolutionarily conserved intracellular protein that blocks DNA synthesis in normal fibroblasts and HeLa cells
TLDR
The cloning and analysis of cDNA for prohibitin reveals that the prohibitin gene appears to be the mammalian analog of Cc, a Drosophila gene that is vital for normal development.
Cell cycle activity and expression of prohibitin mRNA
TLDR
It is suggested that endogenous prohibitin contributes to the control of the G1 to S transition in cycling cells in a complex manner, which involves both a transcriptional and posttranslational mechanism.
Replicative senescence: the human fibroblast comes of age.
TLDR
Identification of participating genes and clarification of their mechanisms of action will help to elucidate the universal cellular decline of biological aging and an important obverse manifestation, the rare escape of cells from senescence leading to immortalization and oncogenesis.
Failure to phosphorylate the retinoblastoma gene product in senescent human fibroblasts.
TLDR
These findings, combined with the observations that T antigen, E1A, and E7 form complexes with, and presumably inactivate, unphosphorylated p110Rb, suggest that failure to phosphorylate p 110Rb may be an immediate cause of failure to enter S phase in senescent HDF.
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