Identification of invasion specific splice variants of the cytoskeletal protein Mena present in mammary tumor cells during invasion in vivo. - Wikidata - wikimedia - TriplyDB

Identification of invasion specific splice variants of the cytoskeletal protein Mena present in mammary tumor cells during invasion in vivo.

Identification of invasion specific splice variants of the cytoskeletal protein Mena present in mammary tumor cells during invasion in vivo.

http://www.wikidata.org/entity/Q34592450

about

Mena deficiency delays tumor progression and decreases metastasis in polyoma middle-T transgenic mouse mammary tumors Molecular insights on context-specific role of profilin-1 in cell migration Epithelial-mesenchymal transition: focus on metastatic cascade, alternative splicing, non-coding RNAs and modulating compounds Correlated immunohistochemical and cytological assays for the prediction of hematogenous dissemination of breast cancer Signatures of breast cancer metastasis at a glance Actin cytoskeletal control during epithelial to mesenchymal transition: focus on the pancreas and intestinal tract Chemotaxis in cancer 5'-Inositol phosphatase SHIP2 recruits Mena to stabilize invadopodia for cancer cell invasion.Direct visualization of the phenotype of hypoxic tumor cells at single cell resolution in vivo using a new hypoxia probe.Identification and expression analysis of splice variants of mouse enabled homologue during development and in adult tissues.Blood vessel endothelium-directed tumor cell streaming in breast tumors requires the HGF/C-Met signaling pathway.Selective gene-expression profiling of migratory tumor cells in vivo predicts clinical outcome in breast cancer patients.The cooperation between hMena overexpression and HER2 signalling in breast cancer Tumor microenvironment of metastasis and risk of distant metastasis of breast cancer.Targeted inactivation of Snail family EMT regulatory factors by a Co(III)-Ebox conjugate.Mammary gland ECM remodeling, stiffness, and mechanosignaling in normal development and tumor progression Invasive breast carcinoma cells from patients exhibit MenaINV- and macrophage-dependent transendothelial migration.Mena invasive (MenaINV) promotes multicellular streaming motility and transendothelial migration in a mouse model of breast cancer Tumor microenvironment of metastasis in human breast carcinoma: a potential prognostic marker linked to hematogenous dissemination Menacalc, a quantitative method of metastasis assessment, as a prognostic marker for axillary node-negative breast cancer.Fe65 Suppresses Breast Cancer Cell Migration and Invasion through Tip60 Mediated Cortactin Acetylation Translocated in liposarcoma regulates the distribution and function of mammalian enabled, a modulator of actin dynamics.A specific FMNL2 isoform is up-regulated in invasive cells Mena invasive (Mena(INV)) and Mena11a isoforms play distinct roles in breast cancer cell cohesion and association with TMEM Post-transcriptional regulation in cancer progression : Microenvironmental control of alternative splicing and translation.Splicing program of human MENA produces a previously undescribed isoform associated with invasive, mesenchymal-like breast tumors.Mena binds α5 integrin directly and modulates α5β1 function.Selectivity in subunit composition of Ena/VASP tetramers.Expression and Distribution Characteristics of Human Ortholog of Mammalian Enabled (hMena) in Glioma Characterization of the expression of the pro-metastatic Mena(INV) isoform during breast tumor progression Tumor Cell-Driven Extracellular Matrix Remodeling Drives Haptotaxis during Metastatic Progression.A Mena invasion isoform potentiates EGF-induced carcinoma cell invasion and metastasis Oncogenic alternative splicing switches: role in cancer progression and prospects for therapy.Posttranscriptional regulation by RNA-binding proteins during epithelial-to-mesenchymal transition.MenaINV mediates synergistic cross-talk between signaling pathways driving chemotaxis and haptotaxis.Mena(INV) dysregulates cortactin phosphorylation to promote invadopodium maturation.Macrophage-dependent tumor cell transendothelial migration is mediated by Notch1/MenaINV-initiated invadopodium formation.Exo70 isoform switching upon epithelial-mesenchymal transition mediates cancer cell invasion.Quantitative assessment of invasive mena isoforms (Menacalc) as an independent prognostic marker in breast cancer.Invading one step at a time: the role of invadopodia in tumor metastasis.

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P2860

Identification of invasion specific splice variants of the cytoskeletal protein Mena present in mammary tumor cells during invasion in vivo.

http://www.wikidata.org/entity/Q34592450

description

2008 nî lūn-bûn

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2008 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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name

Identification of invasion spe ...... cells during invasion in vivo.

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Identification of invasion spe ...... cells during invasion in vivo.

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Identification of invasion spe ...... cells during invasion in vivo.

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Identification of invasion spe ...... cells during invasion in vivo.

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Identification of invasion spe ...... cells during invasion in vivo.

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Identification of invasion spe ...... cells during invasion in vivo.

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Clinical & Experimental Metastasis

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Identification of invasion spe ...... cells during invasion in vivo

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Antonia Patsialou

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Daqian Sun

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Frank B Gertler

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Jacob Avraham

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John S Condeelis

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Sumanta Goswami

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Ulrike Philippar

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Weigang Wang

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P2860

The VASP tetramerization domain is a right-handed coiled coil based on a 15-residue repeat

Ena/VASP proteins enhance actin polymerization in the presence of barbed end capping proteins

Structure of the enabled/VASP homology 1 domain-peptide complex: a key component in the spatial control of actin assembly

Tes, a specific Mena interacting partner, breaks the rules for EVH1 binding

Human Mena protein, a serex-defined antigen overexpressed in breast cancer eliciting both humoral and CD8+ T-cell immune response

Mena, a relative of VASP and Drosophila Enabled, is implicated in the control of microfilament dynamics

Antagonism between Ena/VASP proteins and actin filament capping regulates fibroblast motility

Critical roles of phosphorylation and actin binding motifs, but not the central proline-rich region, for Ena/vasodilator-stimulated phosphoprotein (VASP) function during cell migration.

Ena/VASP proteins can regulate distinct modes of actin organization at cadherin-adhesive contacts.

Molecular cloning of hMena (ENAH) and its splice variant hMena+11a: epidermal growth factor increases their expression and stimulates hMena+11a phosphorylation in breast cancer cell lines.

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Francesca Di Modugno

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