Role of JNK in a Trp53-dependent mouse model of breast cancer. - Wikidata - wikimedia - TriplyDB

Role of JNK in a Trp53-dependent mouse model of breast cancer.

Role of JNK in a Trp53-dependent mouse model of breast cancer.

http://www.wikidata.org/entity/Q33683349

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JNK signalling in cancer: in need of new, smarter therapeutic targets Co-Targeting of JNK and HUNK in Resistant HER2-Positive Breast Cancer Molecular mechanisms of liver injury and hepatocarcinogenesis: focusing on the role of stress-activated MAPK Inflammation- and stress-related signaling pathways in hepatocarcinogenesis JNK2 downregulation promotes tumorigenesis and chemoresistance by decreasing p53 stability in bladder cancer Stress signaling and the shaping of the mammary tissue in development and cancer.Klf4 is a transcriptional regulator of genes critical for EMT, including Jnk1 (Mapk8).Role of JNK in mammary gland development and breast cancer.c-Jun N-terminal kinase 2 prevents luminal cell commitment in normal mammary glands and tumors by inhibiting p53/Notch1 and breast cancer gene 1 expression.In vivo gene manipulation reveals the impact of stress-responsive MAPK pathways on tumor progression.JNK and PTEN cooperatively control the development of invasive adenocarcinoma of the prostate.Recurrent MLK4 Loss-of-Function Mutations Suppress JNK Signaling to Promote Colon Tumorigenesis.Mechanisms that link the oncogenic epithelial-mesenchymal transition to suppression of anoikis.BRAF inhibitors suppress apoptosis through off-target inhibition of JNK signaling.The 2 Faces of JNK Signaling in Cancer.Cdc42 and Rac1 are major contributors to the saturated fatty acid-stimulated JNK pathway in hepatocytes.JNK pathway inhibition enhances chemotherapeutic sensitivity to Adriamycin in nasopharyngeal carcinoma cells.Novel tumor-suppressor function of KLF4 in pediatric T-cell acute lymphoblastic leukemia.Neddylation controls basal MKK7 kinase activity in breast cancer cells.Impaired JNK signaling cooperates with KrasG12D expression to accelerate pancreatic ductal adenocarcinoma.Conflicting evidence for the role of JNK as a target in breast cancer cell proliferation: Comparisons between pharmacological inhibition and selective shRNA knockdown approaches.The cJUN NH2-terminal kinase (JNK) pathway contributes to mouse mammary gland remodeling during involution.The cJUN NH2-terminal kinase (JNK) signaling pathway promotes genome stability and prevents tumor initiation.

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Role of JNK in a Trp53-dependent mouse model of breast cancer.

http://www.wikidata.org/entity/Q33683349

description

2010 nî lūn-bûn

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2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Role of JNK in a Trp53-dependent mouse model of breast cancer.

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Role of JNK in a Trp53-dependent mouse model of breast cancer.

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Role of JNK in a Trp53-dependent mouse model of breast cancer.

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Role of JNK in a Trp53-dependent mouse model of breast cancer.

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Role of JNK in a Trp53-dependent mouse model of breast cancer.

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Role of JNK in a Trp53-dependent mouse model of breast cancer.

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Role of JNK in a Trp53-dependent mouse model of breast cancer.

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P2093

Claire R Weston

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Cristina Cellurale

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D Joseph Jerry

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David S Garlick

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Hayla K Sluss

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Judith Reilly

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Roger J Davis

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The genomic landscapes of human breast and colorectal cancers

Signal transduction by the JNK group of MAP kinases

Human mitogen-activated protein kinase kinase 4 as a candidate tumor suppressor

Alterations in pancreatic, biliary, and breast carcinomas support MKK4 as a genetically targeted tumor suppressor gene

Role of mitogen-activated protein kinase kinase 4 in cancer

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

Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway

Tumor spectrum analysis in p53-mutant mice

Jnk2 effects on tumor development, genetic instability and replicative stress in an oncogene-driven mouse mammary tumor model.

The Jun kinase 2 isoform is preferentially required for epidermal growth factor-induced transformation of human A549 lung carcinoma cells.

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