E-cadherin expression is regulated by miR-192/215 by a mechanism that is independent of the profibrotic effects of transforming growth factor-beta - Wikidata - thesis-toulmin - TriplyDB

E-cadherin expression is regulated by miR-192/215 by a mechanism that is independent of the profibrotic effects of transforming growth factor-beta

E-cadherin expression is regulated by miR-192/215 by a mechanism that is independent of the profibrotic effects of transforming growth factor-beta

http://www.wikidata.org/entity/Q33930316

about

Early detection of diabetic kidney disease: Present limitations and future perspectives MicroRNAs in Diabetic Nephropathy: From Biomarkers to Therapy Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction?Role of regulatory micro RNAs in type 2 diabetes mellitus-related inflammation TGF-β/Smad signaling in renal fibrosis MicroRNAs in Diabetic Kidney Disease Genetics and Epigenetics of Diabetic Nephropathy Mini-review: emerging roles of microRNAs in the pathophysiology of renal diseases microRNAs in kidneys: biogenesis, regulation, and pathophysiological roles Involvement of YAP, TAZ and HSP90 in contact guidance and intercellular junction formation in corneal epithelial cells TGFβ-stimulated microRNA-21 utilizes PTEN to orchestrate AKT/mTORC1 signaling for mesangial cell hypertrophy and matrix expansion microRNA in the development of diabetic complications.Dedifferentiation of immortalized human podocytes in response to transforming growth factor-β: a model for diabetic podocytopathy.MicroRNA-192 suppresses liver metastasis of colon cancer.A novel network profiling analysis reveals system changes in epithelial-mesenchymal transition Hypoxia-induced down-regulation of microRNA-34a promotes EMT by targeting the Notch signaling pathway in tubular epithelial cells.The role of microRNAs in diabetic nephropathy.Post-transcriptional up-regulation of Tsc-22 by Ybx1, a target of miR-216a, mediates TGF-{beta}-induced collagen expression in kidney cells.Changes in the gene expression programs of renal mesangial cells during diabetic nephropathy microRNAs and cancer metabolism reprogramming: the paradigm of metformin miR-200a Prevents renal fibrogenesis through repression of TGF-β2 expression.Identification of a stem-like cell population by exposing metastatic breast cancer cell lines to repetitive cycles of hypoxia and reoxygenation Functional implications of microRNA-215 in TGF-β1-induced phenotypic transition of mesangial cells by targeting CTNNBIP1.miR-200 family expression is downregulated upon neoplastic progression of Barrett's esophagus.Involvement of renal corpuscle microRNA expression on epithelial-to-mesenchymal transition in maternal low protein diet in adult programmed rats Epigenetic mechanisms in diabetic vascular complications.Diabetes complications: the microRNA perspective.Shielding the messenger (RNA): microRNA-based anticancer therapies.MicroRNAs in renal fibrosis.MicroRNA-21 orchestrates high glucose-induced signals to TOR complex 1, resulting in renal cell pathology in diabetes.Implications of microRNAs in colorectal cancer development, diagnosis, prognosis, and therapeutics.Translational study of microRNAs and its application in kidney disease and hypertension research.Systems biology of kidney diseases.miRNA profiling in metastatic renal cell carcinoma reveals a tumour-suppressor effect for miR-215 Epigenetic mechanisms of endothelial dysfunction in type 2 diabetes.Low-dose paclitaxel ameliorates fibrosis in the remnant kidney model by down-regulating miR-192.Suppression of microRNA-29 expression by TGF-β1 promotes collagen expression and renal fibrosis Inhibiting microRNA-192 ameliorates renal fibrosis in diabetic nephropathy.MicroRNAs and the glomerulus A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells

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P2860

E-cadherin expression is regulated by miR-192/215 by a mechanism that is independent of the profibrotic effects of transforming growth factor-beta

http://www.wikidata.org/entity/Q33930316

description

2010 nî lūn-bûn

@nan

2010 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի ապրիլին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

E-cadherin expression is regul ...... ransforming growth factor-beta

@ast

E-cadherin expression is regul ...... ransforming growth factor-beta

@en

type

label

E-cadherin expression is regul ...... ransforming growth factor-beta

@ast

E-cadherin expression is regul ...... ransforming growth factor-beta

@en

prefLabel

E-cadherin expression is regul ...... ransforming growth factor-beta

@ast

E-cadherin expression is regul ...... ransforming growth factor-beta

@en

P1433

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P1476

E-cadherin expression is regul ...... ransforming growth factor-beta

@en

P2093

Bo Wang

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

Gregory J Goodall

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

Karin Jandeleit-Dahm

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

Mark E Cooper

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

Michal Herman-Edelstein

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

Moin Saleem

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

Philip Koh

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

Phillip Kantharidis

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

Stephen M Twigg

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

Wendy Burns

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

P2860

Epithelial-mesenchymal transition and its implications for fibrosis

The miR-200 family inhibits epithelial-mesenchymal transition and cancer cell migration by direct targeting of E-cadherin transcriptional repressors ZEB1 and ZEB2

A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells

The epithelial-mesenchymal transition: new insights in signaling, development, and disease

The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1

The snail superfamily of zinc-finger transcription factors

Overexpression of the microRNA hsa-miR-200c leads to reduced expression of transcription factor 8 and increased expression of E-cadherin

Advanced glycation end products cause epithelial-myofibroblast transdifferentiation via the receptor for advanced glycation end products (RAGE)

Hepatocyte-specific Smad7 expression attenuates TGF-beta-mediated fibrogenesis and protects against liver damage

Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype?

P304

1794-1802

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

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scholarly article

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10.2337/DB09-1736

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7

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59

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43148097

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20393144

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2889781

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