Mouse Thrombospondin-2(THBS2) ELISA kit
Referencia CSB-EL023488MO-96T
embalaje : 96T
Marca : Cusabio
| Size | 96T,5×96T,10×96T |
| Promotion | |
Product Details
Intra-assay Precision (Precision within an assay): CV%<8% | |||||
Three samples of known concentration were tested twenty times on one plate to assess. | |||||
Inter-assay Precision (Precision between assays): CV%<10% | |||||
Three samples of known concentration were tested in twenty assays to assess. | |||||
To assess the linearity of the assay, samples were spiked with high concentrations of mouse THBS2 in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay. | ||||||
| Sample | Serum(n=4) | ||||
1:1 | Average % | 96 | ||||
Range % | 90-103 | |||||
1:2 | Average % | 102 | ||||
Range % | 97-106 | |||||
1:4 | Average % | 89 | ||||
Range % | 86-93 | |||||
1:8 | Average % | 94 | ||||
Range % | 89-98 | |||||
The recovery of mouse THBS2 spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section. | ||||||
Sample Type | Average % Recovery | Range | ||||
Serum (n=5) | 103 | 98-107 | ||||
EDTA plasma (n=4) | 95 | 90-111 | ||||
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed. | ||||||
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ng/ml | OD1 | OD2 | Average | Corrected | ||
400 | 2.366 | 2.454 | 2.410 | 2.230 | ||
200 | 1.523 | 1.633 | 1.578 | 1.398 | ||
100 | 0.974 | 0.958 | 0.966 | 0.786 | ||
50 | 0.603 | 0.632 | 0.618 | 0.438 | ||
25 | 0.421 | 0.425 | 0.423 | 0.243 | ||
12.5 | 0.298 | 0.286 | 0.292 | 0.112 | ||
6.25 | 0.233 | 0.250 | 0.242 | 0.062 | ||
0 | 0.179 | 0.180 | 0.180 |
| ||
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Target Background
(From Uniprot)
- Data provide evidence that TSP2 transcription is suppressed by hypoxia through a mechanism that requires HIF-1alpha.
- TWIST2 induces miR-221-3p expression and consequently suppresses its direct target, THBS2, in lymphatic metastasis cervical cancer.
- 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-graft region.
- 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.
- astrocyte-derived TSP-2 is critical for the maintenance of physiological MMP-2 and MMP-9 levels during the foreign body response and contributes to the repair of the BBB
- Endothelial nitric oxide synthase controls the expression of the angiogenesis inhibitor thrombospondin 2
- The secreted protein is an autocrine inhibitor of marrow stromal cell proliferation.
- Megakaryocytes require this protein for normal platelet formation and function.
- Thrombospondin 2 regulates cell proliferation induced by Rac1 redox-dependent signaling
- TSP2-null mice provide an animal model to assist in the understanding of the molecular basis of spontaneous, premature softening of the uterine cervix.
- Delay in expression of TSP2 and metalloproteinase 2 in the wounds of aged mice could contribute to their impaired rate of wound healing.
- CD36 mediates the antiangiogenic effect of thrombospondin-2, which is modulated by histidine-rich glycoprotein
- the absence of TSP2 protects against ovariectomy-induced bone loss by two complementary processes: increased formation and decreased resorption.
- Mutations targeting intermodular interfaces or calcium binding destabilize the thrombospondin-2 signature domain.
- TSP-2 was found to be present in some, but not all, annulus cells of the human annulus and the mouse annulus.
- Taken together, our observations support a role for TSP2 as critical determinant of the brain response to biomaterials.
- TSP-2 expression in the heart protects against age-dependent dilated cardiomyopathy.
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