Tensin 1 _ TNS1
- Known as:
- Tensin 1 _ TNS1
- Catalog number:
- Y213551
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Tensin 1 _ TNS1
Related genes to: Tensin 1 _ TNS1
- Gene:
- TNS1 NIH gene
- Name:
- tensin 1
- Previous symbol:
- TNS, MXRA6
- Synonyms:
- DKFZp586K0617, PPP1R155
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-30
- Date modifiied:
- 2016-10-05
Related products to: Tensin 1 _ TNS1
Related articles to: Tensin 1 _ TNS1
- : Cardiac allograft fibrosis is an important limiting factor for long-term graft survival. However, the fibrotic process operating in patients with acute cellular rejection (ACR) remains unclear. We aimed to identify altered serum mRNAs related to cardiac fibrosis in patients with ACR and to evaluate their diagnostic accuracy in detecting rejection episodes. : We included 40 serum samples from recipients of transplants undergoing routine endomyocardial biopsies. : Several altered mRNAs associated with fibrosis were detected in patients with ACR. Specifically, the activators of fibroblasts and myofibroblasts (, and ), TGF-β signaling ( and ) and WNT signaling ( and ) pathways were significantly different when we compared grade ≥ 2R ACR and/or grade 1R ACR groups with the nonrejection group. Furthermore, and presented an area under the curve value > 0.90 for identifying patients with moderate and severe grades of cardiac rejection. : In conclusion, we found alterations in the relative abundance of circulating activators of fibroblasts and myofibroblasts, such as or , as well as in major profibrotic pathways, including TGF-β and WNT signaling, especially in clinically relevant cardiac rejection. These findings may contribute to improving the surveillance of patients with cardiac transplant and provide new therapeutic strategies for targeting fibrosis process activation. - Source: PubMed
Publication date: 2026/06/18
Delgado-Arija MartaPérez-Carrillo LorenaGonzález-Torrent IreneGenovés PatriciaGiménez-Escamilla IsaacBenedicto CarlotaMartínez-Dolz LuisPortolés ManuelTarazón EstefaníaRoselló-Lletí Esther - Sphingosine-1-phosphate (S1P) promotes tumor growth and dissemination. Chronic positive feedback communication circuits between cancer and stromal cells involve S1P type-1-receptor (S1PR1) activating cell-type specific signaling networks. We hypothesized that such cell-type specific signaling components would be identifiable by rational, unbiased analysis of public oncogenomic and phosphoproteomic datasets. Guided by S1PR1 expression, we used data mining strategies applied to 32 cancer type datasets of the TCGA oncogenomics program, aiming to identify pan-cancer endothelial and immune S1PR1 signaling partners statistically correlated with patient survival. Gene ontology analysis and unbiased clustering of endothelial and immune S1PR1-signaling partners were used to reveal cell type-specific signaling components that individually and grouped, as transcriptional signatures, were statistically linked to patient survival. Furthermore, the breast cancer CPTAC dataset was analyzed focusing on the signaling phosphoproteome linked to S1PR1 expression. Oncogenic S1PR1 signaling companions included endothelial regulators of cell migration such as Ephexin5, a RhoGEF encoded by the ARHGEF15 gene, and RhoJ, a small Rho GTPase. The immune signaling repertoire linked to S1PR1 expression and patient survival included DOCK2, Vav1 and Rac2. Among the S1PR1 phospho-signaling partners, endothelial ARHGAP24, ARHGAP6, ARHGAP31, and TNS1, and immune ARHGAP25, known to be involved in cytoskeletal reorganization and cell mobilization, clustered as phosphoproteins within a subgroup of breast cancer patients. Given the pharmacological relevance of S1PR1 in endothelial and immune settings, revealing the identity of signaling molecules linked to S1PR1 expression provides useful information to further investigate therapeutic strategies targeting these pathways in the vascular and immune systems. - Source: PubMed
Publication date: 2026/06/20
Torres-Santos YazminBeltrán-Navarro Yarely MabellReyes-Cruz GuadalupeVázquez-Prado José - Integrin adhesion complexes mediate dynamic cell-matrix interactions to regulate cell adhesion, migration and invasion. While increasing evidence suggests that adhesion components can undergo liquid-liquid phase separation, the functional relevance of adhesion-derived condensates remains elusive. Here, we demonstrate that tensin 1 (TNS1), a multidomain adaptor protein linking active integrins with the actin cytoskeleton, forms condensates in cells to regulate adhesion component availability. We show that endogenous TNS1 condensates are formed upon focal adhesion disassembly or limited integrin-extracellular matrix engagement, acting as reversible reservoirs for unphosphorylated adhesion proteins. We identify the TNS1 intrinsically disordered region as governing TNS1 condensation and condensate biophysical properties. We further demonstrate a negative regulatory role for phosphorylation on condensate assembly upon stress-responsive kinase activation. Finally, we confirm the functional effects of TNS1 condensation on adhesion dynamics and cell migration, identifying a feedback loop acutely regulating kinase-mediated adhesion turnover upon integrin activation. - Source: PubMed
Publication date: 2026/06/05
Dibus MichalChastney Megan REnkavi GirayFollain GautierJoshi OmkarVattulainen IlpoIvaska Johanna - To integrate multiscale embedded gene co-expression network analysis (MEGENA) and Mendelian randomisation (MR) to identify new pathogenic factors associated with breast cancer (BC). - Source: PubMed
Wang YangXie RuiZhang HuimingGe Zhicheng - Vascular smooth muscle cell (VSMC) phenotype switching plays a significant role in the pathogenesis of atherosclerosis (AS). However, the subtypes of VSMC transdifferentiation and their impact on AS progression and atherosclerotic plaque instability remains unclear. - Source: PubMed
Yang ShuangFu RuiRen XiaoxiaoSun MengyiLi ZhifanChen ShufengYang BinShi NaYe JueShen ChenyangWang XianqiangCui YongchunWu NaqiongLu XiangfengGu DongfengWang Laiyuan