C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent. - Wikidata - awgldk - TriplyDB

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

http://www.wikidata.org/entity/Q36380929

about

Polycystin-1 and polycystin-2 regulate the cell cycle through the helix-loop-helix inhibitor Id2 BP1 is a negative modulator of definitive erythropoiesis Pkd1 transgenic mice: adult model of polycystic kidney disease with extrarenal and renal phenotypes.Mechanisms of apoptosis by c-Myc.Caspase inhibition reduces tubular apoptosis and proliferation and slows disease progression in polycystic kidney disease MYC and the control of apoptosis.Genetic mechanisms and signaling pathways in autosomal dominant polycystic kidney disease.Ionizing radiation induces caspase-dependent but Chk2- and p53-independent cell death in Drosophila melanogaster.MYC, Cell Competition, and Cell Death in Cancer: The Inseparable Triad.TRPP2 channels regulate apoptosis through the Ca2+ concentration in the endoplasmic reticulum c-Myc induction of programmed cell death may contribute to carcinogenesis: a perspective inspired by several concepts of chemical carcinogenesis.Polycystins and cellular Ca2+ signaling.Role of apoptosis in the development of autosomal dominant polycystic kidney disease (ADPKD).Cellular activation triggered by the autosomal dominant polycystic kidney disease gene product PKD2 c-Myc is necessary for DNA damage-induced apoptosis in the G(2) phase of the cell cycle.Bcl-2 and c-Myc co-operate in the Epstein-Barr virus-immortalized human B-cell line GM607 but do not confer tumorigenicity.p19ARF directly and differentially controls the functions of c-Myc independently of p53.Transcriptional activation of TRADD mediates p53-independent radiation-induced apoptosis of glioma cells.c-Myc antagonizes the effect of p53 on apoptosis and p21WAF1 transactivation in K562 leukemia cells.The roles of caspase-3 and bcl-2 in chemically-induced apoptosis but not necrosis of renal epithelial cells.Overexpression of PKD1 causes polycystic kidney disease.Pituitary tumor transforming gene causes aneuploidy and p53-dependent and p53-independent apoptosis.Murine Pkd1 is a developmentally regulated gene from morula to adulthood: role in tissue condensation and patterning.Organoid cystogenesis reveals a critical role of microenvironment in human polycystic kidney disease.Acute kidney injury induces hallmarks of polycystic kidney disease.Aldosterone promotes proximal tubular cell apoptosis: role of oxidative stress.

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P2860

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

http://www.wikidata.org/entity/Q36380929

description

1997 nî lūn-bûn

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1997年の論文

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1997年学术文章

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1997年学术文章

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1997年学术文章

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1997年学术文章

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1997年学术文章

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1997年學術文章

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1997年學術文章

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1997年學術文章

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name

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

@ast

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

@en

type

label

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

@ast

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

@en

prefLabel

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

@ast

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

@en

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JEM.186.11.1873

P1433

Journal of Experimental Medicine

P1476

C-myc-induced apoptosis in polycystic kidney disease is Bcl-2 and p53 independent.

@en

P2093

C L'Italien

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J Lanoix

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L Barisoni

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M Desforges

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M J Blouin

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M Trudel

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V D'Agati

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P2860

Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death

Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo

Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L)

Tumor suppressor p53 is a direct transcriptional activator of the human bax gene

Fulminant metanephric apoptosis and abnormal kidney development in bcl-2-deficient mice

Bax-deficient mice with lymphoid hyperplasia and male germ cell death

Targeted disruption of Bcl-2 alpha beta in mice: occurrence of gray hair, polycystic kidney disease, and lymphocytopenia

Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours

Coexpression of MMTV/v-Ha-ras and MMTV/c-myc genes in transgenic mice: synergistic action of oncogenes in vivo.

Apoptotic cell death induced by c-myc is inhibited by bcl-2.

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1873-1884

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10.1084/JEM.186.11.1873

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11

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186

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9382886

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P921

apoptotic process

P932

2199149

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