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The protein encoded by THBS2 belongs to the thrombospondin family. Zusätzlich bieten wir Ihnen Thrombospondin 2 Kits (44) und Thrombospondin 2 Proteine (8) und viele weitere Produktgruppen zu diesem Protein an.
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Mouse (Murine) Monoclonal Thrombospondin 2 Primary Antibody für IF, WB - ABIN968394
Kyriakides, Zhu, Smith, Bain, Yang, Lin, Danielson, Iozzo, LaMarca, McKinney, Ginns, Bornstein: Mice that lack thrombospondin 2 display connective tissue abnormalities that are associated with disordered collagen fibrillogenesis, an increased vascular density, and a bleeding diathesis. in The Journal of cell biology 1998
Show all 3 Pubmed References
Human Polyclonal Thrombospondin 2 Primary Antibody für IF (p), IHC (p) - ABIN872994
Chen, Yao, Zhao, He, Ding, Li, Long: MiR-1246 promotes SiHa cervical cancer cell proliferation, invasion, and migration through suppression of its target gene thrombospondin 2. in Archives of gynecology and obstetrics 2014
data suggest that THBS2 might modulate angiogenesis during wound healing in the horse, which could protect against the disproportionate fibroplasia commonly afflicting limb wounds and leading to the development of exuberant granulation tissue
the combination of THBS2 and CA19-9 yielded a sensitivity of 87% for pancreatic ductal adenocarcinoma in the phase 2b study.
Study found that 2 single nucleotide polymorphisms (rs6422747 and rs6422748) in the THBS2 gene were associated with susceptibility of intervertebral disc degeneration (IDD (zeige COL9A3 Antikörper)) but not severity of IDD (zeige COL9A3 Antikörper) in a Chinese Han population; results indicated that THBS2 gene polymorphisms might be the risk factors for IDD (zeige COL9A3 Antikörper).
TSP-2 enhances the migration of PCa (zeige FLVCR1 Antikörper) cells by increasing MMP-2 (zeige MMP2 Antikörper) expression through down-regulation of miR (zeige MLXIP Antikörper)-376c expression.
we report microRNA-135b (miR (zeige MLXIP Antikörper)-135b), a key regulator of the malignancy, highly expressed in the RC component and promoting MLS cell invasion in vitro and metastasis in vivo through the direct suppression of thrombospondin 2 (THBS2).
High THBS2 expression is associated with lung cancer.
STMN1 (zeige STMN1 Antikörper),COF1 (zeige CFL1 Antikörper) and PAIRBP1 (zeige SERBP1 Antikörper) thus represent proteins associated with proliferative and aggressive tumors of high grades, while TSP2 and POSTN (zeige POSTN Antikörper) were connected to low grade tumors with better prognosis
the tissue levels of THBS2 and LECT-2 (zeige LECT2 Antikörper) may correlate with the stage of atherosclerosis.
THBS2 and THBS4 (zeige THBS4 Antikörper) mRNA are overexpressed in gastric cancer in a Southeast Chinese population.
THBS2, but not COL1A2 (zeige COL1A2 Antikörper) and SPP1 (zeige SPP1 Antikörper), may serve as an indicator of gastric cancer prognosis.
The level of THBS2 in differentiating stem cells, influences chondrogenic differentiation potential.
Data suggest THBS1 (zeige THBS1 Antikörper) expression predominates in luteal endothelial cells; THBS2 expression predominates in luteinized granulosa cells. Luteinization down-regulates expression of THBS1 (zeige THBS1 Antikörper)/THBS2, up-regulates expression of FGF2 (fibroblast growth factor 2 (zeige FGF2 Antikörper)).
TSP-1 (zeige THBS1 Antikörper) and -2 were coordinately expressed in the extravascular compartment of the ovary during early follicle development. VEGF (zeige VEGFA Antikörper) was inversely expressed, with expression increasing as follicles developed.
TSP2 deficiency imparted a brittle phenotype on cortical bone. electron microscopy revealed less intensely stained collagen fibrils with altered morphology in the extracellular matrix assembled by osteoblasts on the anterior surface of TSP2-KO femora.
Enhanced levels of TSP-2 in the skin result in reduced susceptibility to chemically-induced skin carcinogenesis.
in the context of osteoblast differentiation, TSP2 promotes the assembly of a type-I collagen-rich matrix by facilitating pro-collagen processing.
The proposed mechanism for the shift in stem cell fate in fracture healing is that increased vascular density and hence oxygen availability in TSP2-null mice regulates differentiation.
The upregulation of TSP-2 mediated by increased oxidative stress contributes to angiogenesis dysfunction in diabetic bone marrow derived angiogenic cells.
TSP2 is a negative regulator of ischemic fracture healing, and in the absence of TSP2 bone regeneration is enhanced.
Using a TSP-2-knockout mouse model and cardiac cell transplantation, we found significantly reduced fibrosis and increased endothelial cell density in the peri (zeige POSTN Antikörper)-graft region.
TSP1 (zeige GZMA Antikörper)-null and TSP2-null mice have lower IOPs than their WT counterparts. The rate of aqueous turnover suggests that the mechanism is enhanced outflow facility.
the two TSP2 isforms are differentially modulated at injured and noninjured skeletal sites in an animal undergoing fracture healing.
TSP-2 has a protective role against cardiac inflammation, injury, and dysfunction in acute viral myocarditis.
The protein encoded by this gene belongs to the thrombospondin family. It is a disulfide-linked homotrimeric glycoprotein that mediates cell-to-cell and cell-to-matrix interactions. This protein has been shown to function as a potent inhibitor of tumor growth and angiogenesis. Studies of the mouse counterpart suggest that this protein may modulate the cell surface properties of mesenchymal cells and be involved in cell adhesion and migration.
, thrombospondin 2
, corticotropin-induced secreted protein
, transmembrane protein 200A