Interactions of DPP-4 and integrin β1 influences endothelial-to-mesenchymal transition. (Q52954535)

9 May 2018

title

Interactions of DPP-4 and integrin β1 influences endothelial-to-mesenchymal transition. (English)

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9 May 2018

author name string

Sen Shi

1

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9 May 2018

Swayam Prakash Srivastava

2

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9 May 2018

Megumi Kanasaki

3

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9 May 2018

Jianhua He

4

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9 May 2018

Munehiro Kitada

5

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9 May 2018

Takako Nagai

6

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9 May 2018

Kyoko Nitta

7

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9 May 2018

Susumu Takagi

8

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9 May 2018

Keizo Kanasaki

9

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9 May 2018

Daisuke Koya

10

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9 May 2018

language of work or name

English

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publication date

1 April 2015

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9 May 2018

published in

Kidney International

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9 May 2018

volume

88

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9 May 2018

issue

3

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9 May 2018

page(s)

479-489

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9 May 2018

Integrin-mediated type II TGF-β receptor tyrosine dephosphorylation controls SMAD-dependent profibrotic signaling

cites work

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Integrin beta1-mediated matrix assembly and signaling are critical for the normal development and function of the kidney glomerulus

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Loss of β1-integrin from urothelium results in overactive bladder and incontinence in mice: a mechanosensory rather than structural phenotype

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Endothelial-to-mesenchymal transition contributes to cardiac fibrosis

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Dipeptidyl peptidase-4 inhibitors attenuate endothelial function as evaluated by flow-mediated vasodilatation in type 2 diabetic patients.

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Integrin structure, activation, and interactions

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CD26 regulates p38 mitogen-activated protein kinase-dependent phosphorylation of integrin beta1, adhesion to extracellular matrix, and tumorigenicity of T-anaplastic large cell lymphoma Karpas 299.

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TGF-beta1 gene transfer to the mouse colon leads to intestinal fibrosis

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Specific interactions between Smad proteins and AP-1 components determine TGFβ-induced breast cancer cell invasion.

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The oral dipeptidyl peptidase-4 inhibitor sitagliptin increases circulating endothelial progenitor cells in patients with type 2 diabetes: possible role of stromal-derived factor-1alpha.

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Role of Endothelial-Mesenchymal Transition (EndoMT) in the Pathogenesis of Fibrotic Disorders

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CD9 negatively regulates CD26 expression and inhibits CD26-mediated enhancement of invasive potential of malignant mesothelioma cells

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Linagliptin-mediated DPP-4 inhibition ameliorates kidney fibrosis in streptozotocin-induced diabetic mice by inhibiting endothelial-to-mesenchymal transition in a therapeutic regimen

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Fibroblasts in kidney fibrosis emerge via endothelial-to-mesenchymal transition

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RIP-Chip: the isolation and identification of mRNAs, microRNAs and protein components of ribonucleoprotein complexes from cell extracts.

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Interference with TGF-beta signaling by Smad3-knockout in mice limits diabetic glomerulosclerosis without affecting albuminuria.

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Dipeptidyl peptidase IV inhibition activates CREB and improves islet vascularization through VEGF-A/VEGFR-2 signaling pathway

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Transforming growth factor-{beta}1 induces Smad3-dependent {beta}1 integrin gene expression in epithelial-to-mesenchymal transition during chronic tubulointerstitial fibrosis

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Transforming growth factor beta: a central modulator of pulmonary and airway inflammation and fibrosis

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Mice lacking Smad3 are protected against streptozotocin-induced diabetic glomerulopathy

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Identifiers

DOI

10.1038/KI.2015.103

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9 May 2018

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9 May 2018