Loss of Rb activates both p53-dependent and independent cell death pathways in the developing mouse nervous system.
about
Functional identification of Api5 as a suppressor of E2F-dependent apoptosis in vivop38 phosphorylates Rb on Ser567 by a novel, cell cycle-independent mechanism that triggers Rb-Hdm2 interaction and apoptosisNegative regulation of DNA replication by the retinoblastoma protein is mediated by its association with MCM7.CDC25A phosphatase is a target of E2F and is required for efficient E2F-induced S phaseThe other side of the coin: the tumor-suppressive aspect of oncogenes and the oncogenic aspect of tumor-suppressive genes, such as those along the CCND-CDK4/6-RB axisPutting the pieces together: How is the mitochondrial pathway of apoptosis regulated in cancer and chemotherapy?The retinoblastoma gene pathway regulates the postmitotic state of hair cells of the mouse inner ear.The closely related transcription factors Sox4 and Sox11 function as survival factors during spinal cord developmentProteomic analysis of pRb loss highlights a signature of decreased mitochondrial oxidative phosphorylationRb deletion in mouse mammary progenitors induces luminal-B or basal-like/EMT tumor subtypes depending on p53 status.E2F3 is a mediator of DNA damage-induced apoptosis.The retinoblastoma tumor-suppressor gene, the exception that proves the ruleE2F4 cooperates with pRB in the development of extra-embryonic tissues.Inhibition of cyclin D1 kinase activity is associated with E2F-mediated inhibition of cyclin D1 promoter activity through E2F and Sp1.Id2 promotes apoptosis by a novel mechanism independent of dimerization to basic helix-loop-helix factors.Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation.p53 facilitates pRb cleavage in IL-3-deprived cells: novel pro-apoptotic activity of p53.Expression of cyclins E1 and E2 during mouse development and in neoplasiaDisruption of retinoblastoma protein family function by human papillomavirus type 16 E7 oncoprotein inhibits lens development in part through E2F-1.Selective inactivation of p53 facilitates mouse epithelial tumor progression without chromosomal instability.Targeted point mutations of p53 lead to dominant-negative inhibition of wild-type p53 functionApoptotic threshold is lowered by p53 transactivation of caspase-6Cell-autonomous and non-cell-autonomous functions of the Rb tumor suppressor in developing central nervous system.Coupling of caspase-9 to Apaf1 in response to loss of pRb or cytotoxic drugs is cell-type-specific.Inhibitors of histone deacetylases target the Rb-E2F1 pathway for apoptosis induction through activation of proapoptotic protein Bim.E2F1 induces phosphorylation of p53 that is coincident with p53 accumulation and apoptosis.ARF differentially modulates apoptosis induced by E2F1 and Myc.Intrauterine ischemic reperfusion switches the fetal transcriptional pattern from HIF-1α- to P53-dependent regulation in the murine brainElevated poly-(ADP-ribose)-polymerase activity sensitizes retinoblastoma-deficient cells to DNA damage-induced necrosisConditional mutation of Rb causes cell cycle defects without apoptosis in the central nervous system.Cell-nonautonomous function of the retinoblastoma tumour suppressor protein: new interpretations of old phenotypes.E2F3 contributes both to the inappropriate proliferation and to the apoptosis arising in Rb mutant embryosp53, Stem Cells, and Reprogramming: Tumor Suppression beyond Guarding the Genome.Adenoviral-E2F-1 radiosensitizes p53wild-type and p53null human prostate cancer cells.K-ras is an essential gene in the mouse with partial functional overlap with N-ras.DPL-1 DP, LIN-35 Rb and EFL-1 E2F act with the MCD-1 zinc-finger protein to promote programmed cell death in Caenorhabditis elegans.Alterations in G(1) to S phase cell-cycle regulators during amyotrophic lateral sclerosis.E2F3 loss has opposing effects on different pRB-deficient tumors, resulting in suppression of pituitary tumors but metastasis of medullary thyroid carcinomasHypoxic stress underlies defects in erythroblast islands in the Rb-null mouse.Cockayne syndrome exhibits dysregulation of p21 and other gene products that may be independent of transcription-coupled repair.
P2860
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P2860
Loss of Rb activates both p53-dependent and independent cell death pathways in the developing mouse nervous system.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年学术文章
@wuu
1996年学术文章
@zh-cn
1996年学术文章
@zh-hans
1996年学术文章
@zh-my
1996年学术文章
@zh-sg
1996年學術文章
@yue
1996年學術文章
@zh
1996年學術文章
@zh-hant
name
Loss of Rb activates both p53- ...... veloping mouse nervous system.
@en
type
label
Loss of Rb activates both p53- ...... veloping mouse nervous system.
@en
prefLabel
Loss of Rb activates both p53- ...... veloping mouse nervous system.
@en
P2093
P2860
P1433
P1476
Loss of Rb activates both p53- ...... veloping mouse nervous system.
@en
P2093
P2860
P304
P407
P577
1996-11-01T00:00:00Z