Thrombospondin-1 Antibodies

Thrombospondin-1 (THBS1)

Adhesive glycoprotein that mediates cell-to-cell and cell-to-matrix interactions. Binds heparin.

May play a role in dentinogenesis and/or upkeep of dentin and dental pulp (By similarity). Ligand for CD36 mediating antiangiogenic properties.

Gene Information

Human
Gene Name:	THBS1
Uniprot:	P07996
Entrez:	7057

Family

Belongs to:
thrombospondin family

Alternative Names

THBS; THBS1; THBS-1; thrombospondin 1; Thrombospondin1; Thrombospondin-1; thrombospondin-1p180; TSP-1; TSP1thrombospondin-1; TSPTSP-1

Molecular Weight

Mass (kDA):
129.383 kDA

Genomic Context

Human
Location:	15q14
Sequence:	15; NC_000015.10 (39581079..39599466)

Subcellular Localizations

Secreted. Cell surface. Secreted, extracellular space, extracellular matrix. Endoplasmic reticulum. Sarcoplasmic reticulum. Secreted by thrombin-activated platelets and binds to the cell surface in the presence of extracellular Ca(2+) (PubMed:6777381). Incorporated into the extracellular matrix of fibroblasts (PubMed:6341993). Also detected in the endoplasmic reticulum and sarcoplasmic reticulum where it plays a role in the ER stress response (By similarity).

Diseases

• Neoplasms
• Malignant Neoplasms
• Carcinoma
• Tumor Angiogenesis
• Cell Transformation, Neoplastic
• Carcinogenesis
• Colorectal Cancer
• Colorectal Neoplasms
• Neoplasm Metastasis
• Adenoma
• Adenocarcinoma
• Malignant Neoplasm Of Stomach
• Stomach Neoplasms

• Inflammation
• Tissue Adhesions
• Malignant Neoplasm Of Breast
• Microsatellite Instability
• Malignant Paraganglionic Neoplasm
• Kidney Diseases
• Mammary Neoplasms

Interacting Proteins

• CD36
• FN1
• HTRA1
• PCOLCE
• TGFB1

Pathways

• Methylation
• Angiogenesis
• Dna Methylation
• Pathogenesis
• Cell Growth
• Cell Proliferation
• Cell Adhesion
• Cell Migration
• Cell Cycle
• Mismatch Repair
• Dna Hypermethylation
• Gene Silencing
• Aging

• Immune Response
• Cell Activation
• Cellular Process
• Coagulation
• Regulation Of Gene Expression
• Inflammatory Response
• Fibrinolysis

PTMs

• Methylation
• Phosphorylation

• Acetylation
• Demethylation

• Cleavage

Research Areas

• Cancer

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/THBS1

Best Uses Of The THBS1 Marker

The molecular biomarker THBS1 is becoming more and more sought-after. It can prevent the development and metastasis LSCC. Additionally the THBS1 marker is able to block the VEGF-angiogenic signaling pathways. Continue reading to learn more. This biomarker will let you know what to expect.

THBS1 stops the development and metastasis LSCC

Recent research has revealed the role of THBS1 for the progression of LSCC. A number of LSCC specimens from patients who had advanced TNM stages were found to have aberrant methylation. This gene is known to stimulate angiogenesis and tumorigenesis. While the significance of this gene in LSCC development is unclear The downregulation of THBS1 in this disease might be involved.

The study examined the expression levels of mRNA and proteins for THBS1 in 66 samples taken from LSCC tumors and adjacent non-tumorous tissues. The levels of THBS-1 proteins were significantly lower in LSCC cancers than their counterparts in non-tumorous tissues. Moreover, tumor-derived THBS-1 expression was significantly lower than that in non-tumorous tissue adjacent to it.

The protein Thrombin-1, which has both stimulatory and inhibitory effects on various forms of cancer, is known as Thrombin-1. The most common mechanism of gene silencing is DNA methylation. Cancer-related development has been extensively studied DNA methylation status. Although the role of THBS-1 remains evident, a recent study has demonstrated that metastasis to tumors in the tumor nodes can be associated with decreased expression of THBS-1's mRNA and protein.

The mOMECs were treated with human THBS1 protein at a concentration of 0.001-1 millimol or no treatment. Then they were stained using the eosin and hematoxylin for identification of the presence of sprouts. The cells were then measured and photographed to determine the number of sprouts per beads.

These results demonstrate that THBS1 stops the development and metastasis LSCC. The results are not correlated because the amount of eggs differed between groups. Further research is needed to determine which biomarkers are most effective in detecting LSCC and the mechanisms of action for THBS1.

In addition, neutralization of antibody THBS1 blocks angiogenesis. In ovulatory follicules injected with the THBS1 antibody the cells were found close to the basement membrane of the granulosa cell layer. They penetrated 32 +-7% of granulosa cells layer, but they did not join with vessels that supply stromal blood.

Immunostaining with anti-THBS1 antibody prevented the rupture of ovulatory follicles and the release of oocytes. Two of the three oocytes in the anti-THBS1 group were present, which suggests that meiosis has not resumed. The anti-THBS1 antibody also decreased the size of granulosa cells and the percentage of endothelial cells invasion within the follicles. This finding is important to understand how successful ovulation occurs.

It blocks or neutralizes the angiogenic signaling pathways of VEGF.

The current anti-angiogenic treatments are targeting several AngI factors, but the majority of these drugs have minimal or no therapeutic effect. Anti-angiogenic drugs like bevacizumab and etoposide block VEGF signaling by sequestering VEGF extracellularly. Despite their powerful anti-angiogenic effects, these drugs result in a range of negative side effects, such as hemorrhage, clots within the arteries hypertension, and a decrease in wound healing. Additionally there have been reports of posterior leukoencephalopathy syndrome that is reversible, protein in urine, intestinal perforation, and fistulas.

One strategy is to target ERK or Akt independently. THBS1 can target three targets and improve the transmission of signals through one pathway , while reducing it through the other. This mechanism is known as "competition". Consequently, the VEGF-induced pERK can be increased by inhibiting PI3K signals while limiting the PVEGFR2 or PI3K interactions.

The VEGF pathway to angiogenicity is the result of a complex series of interactions between a variety of genes. One of these genes is S1PR1. Its purpose is to block LSS activity and increase the expression of claudin-5 in blood vessels. S1PR1 is also known to regulate VEGF-C signaling in the zebrafish.

The model predicts which cellular targets act to inhibit the activity of pAkt and/or pERK when stimulated with FGF and VEGF. The model can also predict the amount of signaling species in the body that will be used to supplement experiments. The results of this research will also serve as a basis for testing the effectiveness of angiogenesis-based therapies.

The LSS controls the expression and location of Kinases. Kinases regulate the phosphorylation downstream of signaling molecules like VEGF. The THBS1 inhibitor blocks VEGF-induced tube growth, which in turn antagonizes/inhibites VEGF signaling pathways to induce angiogenicity.

The ECM plays a crucial role in wound healing and angiogenesis. After exposure to a variety of stimuli, the ECM is degraded and releases of soluble peptides with either anti-angiogenic or pro-angiogenic activities. This study has identified a number of matrikines which were upregulated in the vivo. These proteins are usually created by proteases, and may be released when there is atherosclerotic plaques.

Endothelial cells can be classified into two kinds: ECFC and CAC. Early EPC and late EPC are the same but differ in their differentiation status and capacity to form colonies. They both contribute to neovascularization, but in different ways however, they share an important paracrine function. The ECFC directly contributes to the process by replacing damaged endothelial cell.

It inhibits angiogenesis.

The thrombospondin clan includes the THBS1 protein. This protein family plays several roles in angiogenesis regulation. However, it is not known if THBS1 may affect human Ovulation and the process of luteinization. In vitro experiments were performed on the cynomolgus macaque, which is used as a model of ovulation. THBS1 stimulates capillary sprout formation as well as the migration and proliferation of endothelial cells.

The THBS1 signal is transmitted via the CD36-mediated AMP pathway and is linked to the inhibition of angiogenesis. Preeclampsia can be caused by THBS1 overregulation. This gene may be therapeutically beneficial for this condition. More research is needed to determine if THBS1 is a suitable therapeutic target in treating cardiovascular diseases.

Boster Bio's THBS1 panel shows that THBS1 is an Integrin Lignand. It is a ligand for the alpha-9/beta-1integrin, activates signaling protein. Blocking alpha-9/beta-1 Integrin may hinder cell proliferation, migration and neovascularization.

In vitro studies reveal that THBS1 increases the formation of capillaries stimulating mOMEC growth and migration. THBS1 treatment of mOMECs resulted into increased sprout formation and growth. This was a dose-dependent. The treatment, however, did not alter the length of the sprouts. The sprouts grew in very small amount, but statistically significant.

THBS1 gene expression is regulated by the primary antibody and the molecule aza-2'-deoxy-cytidine (5-aza-dC) induces the re-expression of THBS1. Treatment with THBS1 is not able to stop the growth or spread of Hep-2 cells. However the THBS1 gene is vital to human cognition and synaptic plasticity.

It is not clear the role that thrombospondin-1 has in the fight against cancer. It may have stimulatory and inhibitory actions in certain cancers. DNA methylation is the most popular method to shut down genes. Numerous studies have examined the role of DNAmethylation in the development of tumors. Despite these findings, there is no clear understanding of how THBS1 regulates laryngeal Squamous Cell carcinoma (LSCC). A small amount of tumor-related studies have revealed that a decrease in the THBS-1 protein as well as mRNA expression is linked to lymph node metastasis.

Researchers have discovered that THBS1 gene expression could affect the syncytialization marker genes in a recent study. This gene is a significant marker of the syncytialization process. Researchers also discovered that THBS1 reduces lung angiogenesis in the tissue, which could be useful in the field of cancer research.