Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human Thrombospondin 1 Anticorps:
anti-Mouse (Murine) Thrombospondin 1 Anticorps:
anti-Rat (Rattus) Thrombospondin 1 Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Cow (Bovine) Monoclonal Thrombospondin 1 Primary Antibody pour BP, ICC - ABIN151527
Cupi, Sarra, De Nitto, Franzè, Marafini, Monteleone, Del Vecchio Blanco, Paoluzi, Di Fusco, Gentileschi, Ortenzi, Colantoni, Pallone, Monteleone: Defective expression of scavenger receptors in celiac disease mucosa. dans PLoS ONE 2014
Show all 7 Pubmed References
Mouse (Murine) Polyclonal Thrombospondin 1 Primary Antibody pour IHC, WB - ABIN3022979
Shen, Cao, Wang, Ma, Zeng, Liu, Li, Tao, Gong, Xie: Hippo component YAP promotes focal adhesion and tumour aggressiveness via transcriptionally activating THBS1/FAK signalling in breast cancer. dans Journal of experimental & clinical cancer research : CR 2018
Human Polyclonal Thrombospondin 1 Primary Antibody pour ELISA, WB - ABIN4359279
Pan, Chang, Chuang, Hung: The nonsteroidal anti-inflammatory drug NS398 reactivates SPARC expression via promoter demethylation to attenuate invasiveness of lung cancer cells. dans Experimental biology and medicine (Maywood, N.J.) 2008
Together with previous evidence implicating LTBP4, the THBS1 modifier locus regulates variants in gene interaction networks in mitigating disease progression in muscular dystrophy.
This study revealed the opposite clinical relevance of TSP-1 and its autoantibody in SLE for the first time. TSP-1 may play an anti-inflammatory and immunoregulatory role in SLE autoimmunity. Its autoantibody was increased more frequently in disease-active patients and was associated with more severe clinical manifestations, which implicated its antagonistic role on TSP-1 and its involvement in the pathogenesis of SLE.
the pathological roles of 4N1K-peptide are different from those of TSP-2, and 4N1K-peptide would be a more useful predictive marker and potential therapeutic target compared to TSP-1 and TSP-2 in patients with Bladder Cancer
The data show that TGFB1 induces THBS1 expression via Smad3 which contributes to the invasive behavior during glioblastoma multiforme expansion.
HtrA1 cleavage of thrombospondin-1 generates a proangiogenic fragment in the polarized retinal pigment epithelial cell model of age-related macular degeneration.
Following Schistosoma exposure, TSP-1 levels in the lung increase, via recruitment of circulating monocytes, while TSP-1 inhibition or knockout bone marrow prevents TGF-beta activation and protects against pulmonary hypertension development.
High THBS1 expression is associated with migration, invasion, and progression of bladder cancer.
intracellular dynamics of the TSP1-induced apoptosis signaling pathway
TSP-1 effectively elevated P. gingivalis LPS-induced inflammation mediated by the NF-kappaB pathway and may be critical for pathology of periodontitis.
These findings indicate that PRR13/THBS1 and TXN expression could be used for the prediction of resistance to treatment of epithelial ovarian cancer patients.
TSP-1 appears to play an accessory role in modulating Mp activity in humans and BlaJ mice in a gender, age and muscle-dependent manner, but is unlikely a primary driver of disease progression of dysferlinopathy.
TSP-4 A387P polymorphism, but not TSP-1 polymorphism, is an independent risk factor for acute myocardial infarction in Egyptians.
Results show that the thrombospondin 1 (TSP1) and its receptor CD47 (CD47) axis selectively regulates NADPH oxidase 1 (Nox1) in the regulation of endothelial senescence and suggest potential targets for controlling the aging process at the molecular level.
15-LOX-1 expression in colon and prostate cancer cells leads to reduced angiogenesis. These changes could be mediated by an increase in the expression of both ICAM-1 and the anti-angiogenic protein TSP-1.
miR-98 can suppress the expression of TSP1 in the peripheral B cells of patients with allergic asthma.
Data indicate correlation between the levels of thrombospondin-1 and overall survival of ovarian cancer patients, suggesting thrombospondin-1 may be used as a prognostic factor in ovarian cancer patients.
Studies show that thrombospondin-1 (Thbs-1), is a prolific contributor to the production and modulation of ROS in large conductance vessels and in the peripheral circulation. Recently, the presence of physiologically relevant circulating Thbs-1 levels was proven to also disrupt vasodilation to nitric oxide (NO) in coronary arterioles from aged animals, negatively impacting coronary blood flow reserve. [review]
Our findings suggest that Rab37-mediated TSP1 secretion in cancer cells suppresses metastasis and angiogenesis via a cross-talk with endothelial cells and reveal a novel component of the vesicular exocytic machinery in tumor microenvironment and tumor progression
TSP-1 strongly potentiated the proliferative and migratory activity of PDGF on mesenchymal stromal cells.
This study demonstrated that THBS! was detected in the serums of Alzheimer disease patients.
neither adipocyte nor myeloid/macrophage-specific deletion of TSP1 affected the development of high-fat diet-induced obesity. Adipocyte-specific deletion of TSP1 did not protect mice from obesity-induced inflammation and IR. Obese mice with myeloid/macrophage loss of TSP1 had reduced macrophage accumulation in fat, which was accompanied with reduced inflammation, improved glucose tolerance and insulin sensitivity.
TSP-1 may be beneficial for maintaining BBB integrity in the early phase and functional recovery in late phase after traumatic brain injury.
In a laser injury-induced thrombosis model, P-selectin modulates thrombus propagation independently of VWF and TSP1
These findings shed light on the mechanisms leading to beta-cell failure during metabolic stress and point to THBS1 as an interesting therapeutic target to prevent oxidative stress in type 2 diabetes.
cultured astrocytes isolated from an Fmr1 knockout (Fmr1 KO) mouse model of Fragile X syndrome displayed a significant decrease in TSP-1 protein expression compared to the wildtype (WT) astrocytes.
In pulmonary hypertension TSP1-CD47 is upregulated, and contributes to pulmonary arterial vasculopathy and dysfunction.
HIF-1alpha induced angiogenesis by upregulating not only vascular endothelial growth factor but also miR-21 via inhibiting a novel target gene TSP-1. Both of them may contribute to the protective effect of HIF-1alpha on renal I/R injury.
the results obtained by combining bioinformatics and preclinical studies strongly suggest that targeting TSP-1/CD47 axis may represent a valuable therapeutic alternative for hampering melanoma spreading.
TSP-1 deficiency promotes maladaptive remodelling of the ECM leading to accelerated abdominal aortic aneurysms progression.
TSP-1 suppressed insulin signaling in cultured muscle cells, which was accompanied by the activation of stress signaling such as JNK, p38, and IKK.
Three transcription factors were overexpressed and eleven underexpressed in TSP1(-/-) compared to WT LGs.
Data indicate that thrombospondin-1 may contribute to a destructive macrophage response in dysferlinopathy and pose the intriguing possibility that thrombospondin-1 levels may serve as a biomarker for disease progression.
demonstrate that HIF-2alpha is clearly implicated in the TSP1 pulmonary regulation and provide new insights on its contribution to pulmonary arterial hypertension-driven vascular remodelling and vasoconstriction
Thrombospondin-1 was differentially expressed according to tumor grade, but not affected by p53 expression or mutational status
Data suggest neutrophil protease- Tsp-1 (thrombospondin-1) axis as a potential antimetastatic therapeutic target.
These results contribute new insights on the controversial role of TSP-1 in cancer.
The accumulation and thereby the functionality of thrombospondin in extracellular matrix is controlled by concentration-dependent, intermolecular "matrix trapping" mechanism.
TSP1 contributes to progression of chronic kidney disease by catalyzing activation of latent TGF-beta1, resulting in promotion of a fibroproliferative response over an inflammatory response.
These data support the contention that FGF2 and TGFB1 modulate THBS1 via miR-221.
temporal expression and localization pattern of the thrombospondins and their specific receptors in the antral follicles and corpora lutea during the different physiological phases of the estrous cycle and induced luteolysis appear to be compatible with their inhibitory role in the control of ovarian angiogenesis
Data suggest THBS1 expression predominates in luteal endothelial cells; THBS2 expression predominates in luteinized granulosa cells. Luteinization down-regulates expression of THBS1/THBS2, up-regulates expression of FGF2 (fibroblast growth factor 2).
role in inducing vascular smooth muscle cell chemotaxis
thrombospondin has a role in regulating the migratory phenotype of endothelial cells and fibroblasts
Thrombospondin has a role in inducing RhoA inactivation through FAK-dependent signaling to stimulate focal adhesion disassembly
Thrombospondin-1 and -2 were coordinately expressed in the extravascular compartment of the ovary during early follicle development. VEGF was inversely expressed, with expression increasing as follicles developed.
Preincubation of erythroid cells with thrombospondin 1 eliminated the inhibitory activity of insulin-like growth factor
The cell-specific regulation of TSP-1 suggests a potential mechanism for the aberrant angiogenesis in diabetics and TSP-1 involvement in development of various vascular diabetic complications
The novel finding that TSP-1-induced migration is dependent on the CD44 receptor links 2 pathways thought to be disparate (ie, TSP-1 and HyA).
These current studies were undertaken to determine how TSP-1 functions to modulate the smooth muscle cell response to IGF-I and the mechanisms by which hyperglycemia regulates TSP-1 protein.
Increased TSP-1 expression in non-heart-beating donors may indicate a compensatory response to the reported diminished TGF-beta1 expression.
ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation
The protein encoded by this gene is a subunit of a disulfide-linked homotrimeric protein. This protein is an adhesive glycoprotein that mediates cell-to-cell and cell-to-matrix interactions. This protein can bind to fibrinogen, fibronectin, laminin, type V collagen and integrins alpha-V/beta-1. This protein has been shown to play roles in platelet aggregation, angiogenesis, and tumorigenesis.
, thrombospondin 1
, thrombospondin 2