TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73. - Wikidata - wikimedia - TriplyDB

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

http://www.wikidata.org/entity/Q35531125

about

Mutant p53 interactome identifies nardilysin as a p53R273H-specific binding partner that promotes invasion Oncogenic Intra-p53 Family Member Interactions in Human Cancers Mutant p53: One, No One, and One Hundred Thousand The rebel angel: mutant p53 as the driving oncogene in breast cancer.Mutant p53 enhances MET trafficking and signalling to drive cell scattering and invasion.Characteristics and survival of patients with advanced cancer and p53 mutations.Pla2g16 phospholipase mediates gain-of-function activities of mutant p53.Targeting TopBP1 at a convergent point of multiple oncogenic pathways for cancer therapy A mutant p53/let-7i-axis-regulated gene network drives cell migration, invasion and metastasis.Gain of function mutant p53 proteins cooperate with E2F4 to transcriptionally downregulate RAD17 and BRCA1 gene expression Mutant p53: one name, many proteins.An interaction between human papillomavirus 16 E2 and TopBP1 is required for optimum viral DNA replication and episomal genome establishment Targeting mutant p53 by a SIRT1 activator YK-3-237 inhibits the proliferation of triple-negative breast cancer cells The consequence of oncomorphic TP53 mutations in ovarian cancer.Akt switches TopBP1 function from checkpoint activation to transcriptional regulation through phosphoserine binding-mediated oligomerization.Ovarian tumour growth is characterized by mevalonate pathway gene signature in an orthotopic, syngeneic model of epithelial ovarian cancer.YAP enhances the pro-proliferative transcriptional activity of mutant p53 proteins.The activating transcription factor 3 protein suppresses the oncogenic function of mutant p53 proteins.Mutant p53 drives pancreatic cancer metastasis through cell-autonomous PDGF receptor β signaling The TP73 complex network: ready for clinical translation in cancer?TP53 mutants in the tower of babel of cancer progression.Mutant p53 in cancer: new functions and therapeutic opportunities.Unravelling mechanisms of p53-mediated tumour suppression.Battle against cancer: an everlasting saga of p53.Mutant p53 upregulates alpha-1 antitrypsin expression and promotes invasion in lung cancer.ID4 regulates transcriptional activity of wild type and mutant p53 via K373 acetylation Mutant p53 perturbs DNA replication checkpoint control through TopBP1 and Treslin.Gain-of-function p53 activates multiple signaling pathways to induce oncogenicity in lung cancer cells.Levels of the E2 interacting protein TopBP1 modulate papillomavirus maintenance stage replication.Regulation of human genome expression and RNA splicing by human papillomavirus 16 E2 protein.Transcriptional Regulation by Wild-Type and Cancer-Related Mutant Forms of p53.Mutant p53 regulates Dicer through p63-dependent and -independent mechanisms to promote an invasive phenotype.Functions of TAp63 and p53 in restraining the development of metastatic cancer.The Deacetylase SIRT1 Regulates the Replication Properties of Human Papillomavirus 16 E1 and E2.p53-R273H upregulates neuropilin-2 to promote cell mobility and tumor metastasis The c.*229C > T gene polymorphism in 3'UTR region of the topoisomerase IIβ binding protein 1 gene and LOH in BRCA1/2 regions and their effect on the risk and progression of human laryngeal carcinoma.Why Human Papillomaviruses Activate the DNA Damage Response (DDR) and How Cellular and Viral Replication Persists in the Presence of DDR Signaling.A rare DNA contact mutation in cancer confers p53 gain-of-function and tumor cell survival via TNFAIP8 induction.Mutant p53 partners in crime.Li-Fraumeni Syndrome Disease Model: A Platform to Develop Precision Cancer Therapy Targeting Oncogenic p53.

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P2860

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

http://www.wikidata.org/entity/Q35531125

description

2011 nî lūn-bûn

@nan

2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի սեպտեմբերին հրատարակված գիտական հոդված

@hy

2011年の論文

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2011年論文

@yue

2011年論文

@zh-hant

2011年論文

@zh-hk

2011年論文

@zh-mo

2011年論文

@zh-tw

2011年论文

@wuu

name

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

@ast

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

@en

type

label

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

@ast

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

@en

prefLabel

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

@ast

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

@en

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Molecular and Cellular Biology

P1476

TopBP1 mediates mutant p53 gain of function through NF-Y and p63/p73.

@en

P2093

Kang Liu

http://www.w3.org/2001/XMLSchema#string

Shiyun Ling

http://www.w3.org/2001/XMLSchema#string

Weei-Chin Lin

http://www.w3.org/2001/XMLSchema#string

P2860

A vertebrate gene, ticrr, is an essential checkpoint and replication regulator

Treslin collaborates with TopBP1 in triggering the initiation of DNA replication

Gain of function of mutant p53: the mutant p53/NF-Y protein complex reveals an aberrant transcriptional mechanism of cell cycle regulation

Regulation of TopBP1 oligomerization by Akt/PKB for cell survival

Analysis of promoter binding by the E2F and pRB families in vivo: distinct E2F proteins mediate activation and repression

TopBP1 recruits Brg1/Brm to repress E2F1-induced apoptosis, a novel pRb-independent and E2F1-specific control for cell survival

The ePHD protein SPBP interacts with TopBP1 and together they co-operate to stimulate Ets1-mediated transcription

Regulation of E2F1 by BRCT domain-containing protein TopBP1

Mutant p53 proteins bind DNA in a DNA structure-selective mode

Structure and function of the Rad9-binding region of the DNA-damage checkpoint adaptor TopBP1

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4464-4481

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scholarly article

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10.1128/MCB.05574-11

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22

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31

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21930790

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3209258

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