Germ line transmission of the Cdk4(R24C) mutation facilitates tumorigenesis and escape from cellular senescence. - Wikidata - wikimedia - TriplyDB

Germ line transmission of the Cdk4(R24C) mutation facilitates tumorigenesis and escape from cellular senescence.

Germ line transmission of the Cdk4(R24C) mutation facilitates tumorigenesis and escape from cellular senescence.

http://www.wikidata.org/entity/Q24540051

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Melanoma: from melanocyte to genetic alterations and clinical options CDK4 and CDK6 delay senescence by kinase-dependent and p16INK4a-independent mechanisms The p400 E1A-associated protein is a novel component of the p53 --> p21 senescence pathway Requirement of Cdk4 for v-Ha-ras-Induced Breast Tumorigenesis and Activation of the v-ras-Induced Senescence Program by the R24C Mutation Current State of Animal (Mouse) Modeling in Melanoma Research Loss of CDKN2A expression is a frequent event in primary invasive melanoma and correlates with sensitivity to the CDK4/6 inhibitor PD0332991 in melanoma cell lines.RB regulates pancreas development by stabilizing Pdx1 Islet biology, the CDKN2A/B locus and type 2 diabetes risk.The Cdk4-E2f1 pathway regulates early pancreas development by targeting Pdx1+ progenitors and Ngn3+ endocrine precursors.Cdk4 regulates recruitment of quiescent beta-cells and ductal epithelial progenitors to reconstitute beta-cell mass Slow and steady is the key to beta-cell replication.G1/S cell cycle arrest provides anoikis resistance through Erk-mediated Bim suppression.Genetically engineered mouse models of pituitary tumors Establishment of functioning human corneal endothelial cell line with high growth potential.Telomere dysfunction suppresses multiple endocrine neoplasia in mice.Cooperativity of Cdk4R24C and Ras in melanoma development.Abolition of cyclin-dependent kinase inhibitor p16Ink4a and p21Cip1/Waf1 functions permits Ras-induced anchorage-independent growth in telomerase-immortalized human fibroblasts.Modeling high-grade serous ovarian carcinogenesis from the fallopian tube Reversible cell cycle inhibition and premature aging features imposed by conditional expression of p16Ink4a.Exploring the tumors of multiple endocrine neoplasia type 1 in mouse models for basic and preclinical studies Oncogenes in melanoma.Transforming growth factor-β adaptor, β2-spectrin, modulates cyclin dependent kinase 4 to reduce development of hepatocellular cancer.Rapid growth of invasive metastatic melanoma in carcinogen-treated hepatocyte growth factor/scatter factor-transgenic mice carrying an oncogenic CDK4 mutation.Association of variants in CDKN2A/2B and CDKAL1 genes with gestational insulin sensitivity and disposition in pregnant Han Chinese women.Of mice and MEN1: Insulinomas in a conditional mouse knockout.Co-expression of p16(INK4A) and laminin 5 gamma2 by microinvasive and superficial squamous cell carcinomas in vivo and by migrating wound and senescent keratinocytes in culture.Cdk4 disruption renders primary mouse cells resistant to oncogenic transformation, leading to Arf/p53-independent senescence.Novel ARF/p53-independent senescence pathways in cancer repression.Retinoblastoma tumor-suppressor protein phosphorylation and inactivation depend on direct interaction with Pin1.Cyclin-Dependent Kinase Inhibitors as Anticancer Therapeutics CDK4: A Key Player in the Cell Cycle, Development, and Cancer Absence of germline CDKN2A mutation in Sicilian patients with familial malignant melanoma: Could it be a population-specific genetic signature?Investigating the specific core genetic-and-epigenetic networks of cellular mechanisms involved in human aging in peripheral blood mononuclear cells.p16INK4a-induced senescence is disabled by melanoma-associated mutations Genetically engineered mouse models for skin research: taking the next step Regulatory mechanisms of tumor suppressor P16(INK4A) and their relevance to cancer.Signaling through cyclin D-dependent kinases.Dissecting Pin1 and phospho-pRb regulation.Exome sequencing identifies recurrent somatic MAP2K1 and MAP2K2 mutations in melanoma.Lack of cyclin-dependent kinase 4 inhibits c-myc tumorigenic activities in epithelial tissues.

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P2860

Germ line transmission of the Cdk4(R24C) mutation facilitates tumorigenesis and escape from cellular senescence.

http://www.wikidata.org/entity/Q24540051

description

2002 nî lūn-bûn

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2002 թուականի Յունուարին հրատարակուած գիտական յօդուած

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Germ line transmission of the ...... scape from cellular senescence

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Germ line transmission of the ...... cape from cellular senescence.

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Germ line transmission of the ...... cape from cellular senescence.

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Germ line transmission of the ...... scape from cellular senescence

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Germ line transmission of the ...... cape from cellular senescence.

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Germ line transmission of the ...... scape from cellular senescence

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Germ line transmission of the ...... cape from cellular senescence.

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Molecular and Cellular Biology

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E Premkumar Reddy

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Richard V Mettus

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Stephen C Cosenza

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Sushil G Rane

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P2860

New functional activities for the p21 family of CDK inhibitors

ARF promotes MDM2 degradation and stabilizes p53: ARF-INK4a locus deletion impairs both the Rb and p53 tumor suppression pathways

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

A biomarker that identifies senescent human cells in culture and in aging skin in vivo

Quantitative studies of the growth of mouse embryo cells in culture and their development into established lines

CDK inhibitors: positive and negative regulators of G1-phase progression

Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia

Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers

A cell cycle regulator potentially involved in genesis of many tumor types

Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes

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