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pRB plays an essential role in cell cycle arrest induced by DNA damage

pRB plays an essential role in cell cycle arrest induced by DNA damage

http://www.wikidata.org/entity/Q36326866

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The retinoblastoma family proteins bind to and activate diacylglycerol kinase zeta DNA-damage-responsive acetylation of pRb regulates binding to E2F-1 Phosphorylation of pRB at Ser612 by Chk1/2 leads to a complex between pRB and E2F-1 after DNA damage p38 phosphorylates Rb on Ser567 by a novel, cell cycle-independent mechanism that triggers Rb-Hdm2 interaction and apoptosis Deacetylation of the retinoblastoma tumour suppressor protein by SIRT1 Phosphorylation of serines 635 and 645 of human Rad17 is cell cycle regulated and is required for G(1)/S checkpoint activation in response to DNA damage E2F integrates cell cycle progression with DNA repair, replication, and G(2)/M checkpoints E2F mediates cell cycle-dependent transcriptional repression in vivo by recruitment of an HDAC1/mSin3B corepressor complex Differential role of RB in response to UV and IR damage.RB1: a prototype tumor suppressor and an enigma Hepatitis C Virus Induces E6AP-Dependent Degradation of the Retinoblastoma Protein Compensation of BRG-1 function by Brm: insight into the role of the core SWI-SNF subunits in retinoblastoma tumor suppressor signaling Pocket proteins and cell cycle control Differential impact of tumor suppressor pathways on DNA damage response and therapy-induced transformation in a mouse primary cell model Combination treatment of tamoxifen with risperidone in breast cancer RB-dependent S-phase response to DNA damage Loss of RBF1 changes glutamine catabolism Altered regulation of cell cycle machinery involved in interleukin-1-induced G(1) and G(2) phase growth arrest of A375S2 human melanoma cells.Separation of anti-proliferation and anti-apoptotic functions of retinoblastoma protein through targeted mutations of its A/B domain.The retinoblastoma tumor-suppressor gene, the exception that proves the rule E2F1 plays a direct role in Rb stabilization and p53-independent tumor suppression.Alternative pathways for the extension of cellular life span: inactivation of p53/pRb and expression of telomerase.Cyclin D activates the Rb tumor suppressor by mono-phosphorylation Destabilization of the retinoblastoma tumor suppressor by human papillomavirus type 16 E7 is not sufficient to overcome cell cycle arrest in human keratinocytes.Inactivation of p21 by E1A leads to the induction of apoptosis in DNA-damaged cells.Functional interactions between retinoblastoma and c-MYC in a mouse model of hepatocellular carcinoma.Hepatitis C virus NS5B protein delays s phase progression in human hepatocyte-derived cells by relocalizing cyclin-dependent kinase 2-interacting protein (CINP).Mitotic chromosome condensation mediated by the retinoblastoma protein is tumor-suppressive Establishment of irreversible growth arrest in myogenic differentiation requires the RB LXCXE-binding function.Effect of high intratesticular estrogen on global gene expression and testicular cell number in rats.Mechanism targeted discovery of antitumor marine natural products.Tailoring to RB: tumour suppressor status and therapeutic response.RORα binds to E2F1 to inhibit cell proliferation and regulate mammary gland branching morphogenesis Distinct mechanisms of E2F regulation by Drosophila RBF1 and RBF2 Mechanism-based screen establishes signalling framework for DNA damage-associated G1 checkpoint response.RB·E2F1 complex mediates DNA damage responses through transcriptional regulation of ZBRK1.DNA damage signals through differentially modified E2F1 molecules to induce apoptosis.Elevated expression of Runx2 as a key parameter in the etiology of osteosarcoma.Overexpression of c-Myc alters G(1)/S arrest following ionizing radiation The role of the RB tumour suppressor pathway in oxidative stress responses in the haematopoietic system.

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pRB plays an essential role in cell cycle arrest induced by DNA damage

http://www.wikidata.org/entity/Q36326866

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1998 nî lūn-bûn

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1998年の論文

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1998年学术文章

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1998年学术文章

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1998年学术文章

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1998年学术文章

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1998年学术文章

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1998年學術文章

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1998年學術文章

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1998年學術文章

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name

pRB plays an essential role in cell cycle arrest induced by DNA damage

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pRB plays an essential role in cell cycle arrest induced by DNA damage

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pRB plays an essential role in cell cycle arrest induced by DNA damage

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pRB plays an essential role in cell cycle arrest induced by DNA damage

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prefLabel

pRB plays an essential role in cell cycle arrest induced by DNA damage

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pRB plays an essential role in cell cycle arrest induced by DNA damage

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PNAS.95.20.11945

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Proceedings of the National Academy of Sciences of the United States of America

P1476

pRB plays an essential role in cell cycle arrest induced by DNA damage

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P2093

E A Harrington

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E Harlow

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J L Bruce

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N Dyson

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P2860

Growth suppression by p18, a p16INK4/MTS1- and p14INK4B/MTS2-related CDK6 inhibitor, correlates with wild-type pRb function

Growth suppression by p16ink4 requires functional retinoblastoma protein

UV irradiation stimulates levels of p53 cellular tumor antigen in nontransformed mouse cells

p53, the cellular gatekeeper for growth and division

WAF1, a potential mediator of p53 tumor suppression

Inhibition of cell proliferation by p107, a relative of the retinoblastoma protein

14-3-3sigma is a p53-regulated inhibitor of G2/M progression

Cyclin-dependent kinases are inactivated by a combination of p21 and Thr-14/Tyr-15 phosphorylation after UV-induced DNA damage

Ras signalling linked to the cell-cycle machinery by the retinoblastoma protein

Effects of p21(Cip1/Waf1) at both the G1/S and the G2/M cell cycle transitions: pRb is a critical determinant in blocking DNA replication and in preventing endoreduplication

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11945-11950

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