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M C Hollander

Researcher at National Institutes of Health

Publications -  18
Citations -  4436

M C Hollander is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Gene & DNA damage. The author has an hindex of 14, co-authored 17 publications receiving 4338 citations.

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Phosphorylation of human p53 by p38 kinase coordinates N‐terminal phosphorylation and apoptosis in response to UV radiation

TL;DR: Results suggest that p38 kinase plays a prominent role in an integrated regulation of N‐terminal phosphorylation that regulates p53‐mediated apoptosis after UV radiation.
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Mammalian genes coordinately regulated by growth arrest signals and DNA-damaging agents.

TL;DR: Five of the gadd cDNA clones encode transcripts that are increased by other growth cessation signals: growth arrest by serum reduction, medium depletion, contact inhibition, or a 24-h exposure to hydroxyurea, suggesting that these genes may represent part of a novel regulatory pathway involved in the negative control of mammalian cell growth.
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GADD45 induction of a G2/M cell cycle checkpoint

TL;DR: Genetic and physiological evidence of a Gadd45-mediated G2/M checkpoint was obtained by using GADD45-deficient human or murine cells, indicating that the mammalian genome is protected by a multiplicity of G 2/M checkpoints in response to specific types of DNA damage.
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DNA damage-inducible transcripts in mammalian cells

TL;DR: Hybridization subtraction at low ratios of RNA to cDNA was used to enrich for the cDNA of transcripts increased in Chinese hamster cells after UV irradiation, and predicted amino acid sequence of one cDNA had two localized areas of homology with the rat helix-destabilizing protein.
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The gadd and MyD genes define a novel set of mammalian genes encoding acidic proteins that synergistically suppress cell growth.

TL;DR: Observations indicate that these genes define a novel class of mammalian genes encoding acidic proteins involved in the control of cellular growth, which are distinguished from other growth arrest genes in that they are DNA damage inducible.