Browse our anti-Thrombospondin 1 (THBS1) Antibodies

Human Thrombospondin 1 (THBS1) interaction partners

1. The high expression of VEGF and the low expression of TSP-1 in breast cancer tissues are significantly correlated with the main clinical features. The recurrence rate of patients with high expression of VEGF and low expression of TSP is high.

2. serum levels decrease in pregnant women presenting with pre-eclampsia

3. Histamine-activated macrophages could locally activate signaling pathways via FAK and THBS1 genes that are effective in the proliferation and migration of vascular smooth muscle cells.

4. TSP-1 provides an additional line of defense by directly subduing host-derived proteolysis, with dose-dependent inhibition of neutrophil elastase from airway neutrophils of mechanically ventilated critically ill patients.

5. PEDF decreases the metastatic potential of non-small cell lung carcinoma cells through regulation of THBS1 release in cancer cell-derived exosomes.

6. TSP-1 level is significantly increased in AD patients and might participate in AD via promoting classically activated macrophage (M1) macrophage differentiation and SMC apoptosis.

7. The EFEMP1, an extracellular matrix protein mutated in Doyne honeycomb retinal dystrophy, a genetic eye disease similar to AMD, and thrombospondin 1 (TSP1), an inhibitor of angiogenesis.

8. Thrombospondin-1 (TSP1) plays an indirect role in collagen homeostasis through interactions with matrix metalloproteinases and transforming growth factor-beta1 (TGF-beta1); TSP1 also affects collagen fibril formation directly.

9. Thbs1 is a critical component of mechanotransduction, as well as a modulator of elastic fiber organization. Maladaptive upregulation of Thbs1 results in disruption of elastin-contractile units and dysregulation of actin cytoskeletal remodeling, contributing to the development of ascending aortic aneurysms.

10. The analysis of a large transcriptomic dataset derived from the tumors of patients with Triple Negative Breast Cancer revealed that the expression of CD163, CXCR4, THBS1 predicted relapse-free survival.

11. Together with previous evidence implicating LTBP4, the THBS1 modifier locus regulates variants in gene interaction networks in mitigating disease progression in muscular dystrophy.

12. 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.

13. 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

14. The data show that TGFB1 induces THBS1 expression via Smad3 which contributes to the invasive behavior during glioblastoma multiforme expansion.

15. HtrA1 cleavage of thrombospondin-1 generates a proangiogenic fragment in the polarized retinal pigment epithelial cell model of age-related macular degeneration.

16. 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.

17. High THBS1 expression is associated with migration, invasion, and progression of bladder cancer.

18. intracellular dynamics of the TSP1-induced apoptosis signaling pathway

19. TSP-1 effectively elevated P. gingivalis LPS-induced inflammation mediated by the NF-kappaB pathway and may be critical for pathology of periodontitis.

20. These findings indicate that PRR13/THBS1 and TXN expression could be used for the prediction of resistance to treatment of epithelial ovarian cancer patients.

Mouse (Murine) Thrombospondin 1 (THBS1) interaction partners

1. We observed an upregulation in the expression of TSP1 and TSP2 mRNA in control mouse cochleae following noise exposure. afferent synaptic counts and auditory brainstem responses (ABRs) in noise-exposed TSP1 and TSP2 knockout (-/-) mice exhibited a worst recovery than controls. TSP1-/- mice showed greater susceptibility to noise-induced hearing loss at low frequencies.

2. Study in mouse pneumonia model shows that thrombospondin-1 (TSP-1) dose-dependently inhibits Pseudomonas aeruginosa (PA) metalloendoprotease LasB, a virulence factor. TSP-1-deficient mice show reduced survival, impaired host defense, and increased lung permeability with exaggerated neutrophil activation following acute intrapulmonary PA infection.

3. In intrinsically photosensitive retinal ganglion cells (ipRGCs), Thbs1 was the most differentially expressed gene during axon regeneration and cell survival.THBS1 knockdown in RGCs eliminated axon regeneration. RGC overexpression of THBS1 enhanced regeneration in both ipRGCs and non-ipRGCs. The trimerization and C-terminal domains promoted regeneration, while the THBS type-1 repeats were dispensable.

4. Thbs1 is a critical component of mechanotransduction, as well as a modulator of elastic fiber organization. Maladaptive upregulation of Thbs1 results in disruption of elastin-contractile units and dysregulation of actin cytoskeletal remodeling, contributing to the development of ascending aortic aneurysms.

5. 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.

6. 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.

7. 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.

8. TSP-1 may be beneficial for maintaining BBB integrity in the early phase and functional recovery in late phase after traumatic brain injury.

9. In a laser injury-induced thrombosis model, P-selectin modulates thrombus propagation independently of VWF and TSP1

10. 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.

11. 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.

12. In pulmonary hypertension TSP1-CD47 is upregulated, and contributes to pulmonary arterial vasculopathy and dysfunction.

13. 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.

14. 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.

15. TSP-1 deficiency promotes maladaptive remodelling of the ECM leading to accelerated abdominal aortic aneurysms progression.

16. TSP-1 suppressed insulin signaling in cultured muscle cells, which was accompanied by the activation of stress signaling such as JNK, p38, and IKK.

17. Three transcription factors were overexpressed and eleven underexpressed in TSP1(-/-) compared to WT LGs.

18. 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.

19. 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

20. Thrombospondin-1 was differentially expressed according to tumor grade, but not affected by p53 expression or mutational status

Cow (Bovine) Thrombospondin 1 (THBS1) interaction partners

1. These data support the contention that FGF2 and TGFB1 modulate THBS1 via miR-221.

2. 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

3. 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).

4. role in inducing vascular smooth muscle cell chemotaxis

5. thrombospondin has a role in regulating the migratory phenotype of endothelial cells and fibroblasts

6. Thrombospondin has a role in inducing RhoA inactivation through FAK-dependent signaling to stimulate focal adhesion disassembly

7. 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.

8. Preincubation of erythroid cells with thrombospondin 1 eliminated the inhibitory activity of insulin-like growth factor

9. 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

10. 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).

Pig (Porcine) Thrombospondin 1 (THBS1) interaction partners

1. miR-222 inhibits pGC apoptosis by targeting THBS1. miR-222 and THBS1 play important roles in follicular atresia, ovarian development, and female reproduction.

2. 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.

3. Increased TSP-1 expression in non-heart-beating donors may indicate a compensatory response to the reported diminished TGF-beta1 expression.

Zebrafish Thrombospondin 1 (THBS1) interaction partners

1. ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation