MST1R Antibodies

Macrophage-stimulating protein receptor (MST1R)

Receptor tyrosine kinase that transduces signals from the extracellular matrix to the cytoplasm by binding to MST1 ligand. Regulates many physiological processes including cell survival, migration and differentiation.

Ligand binding at the cell surface induces autophosphorylation of RON on its intracellular domain that provides docking sites for downstream signaling molecules. After activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1 or the adapter GAB1.

Gene Information

Human
Gene Name:	MST1R
Uniprot:	Q04912
Entrez:	4486

Family

Belongs to:
protein kinase superfamily

Alternative Names

CD136 antigen; CD136; CDw136c-met-related tyrosine kinase; EC 2.7.10; EC 2.7.10.1; macrophage stimulating 1 receptor (c-met-related tyrosine kinase); MSP R; MSP receptor; MSPR; MST1R; p185-Ron; Protein-tyrosine kinase 8; PTK8 protein tyrosine kinase 8; PTK8; Ron; RONmacrophage-stimulating protein receptor; soluble RON variant 1; soluble RON variant 2; soluble RON variant 3; soluble RON variant 4

Molecular Weight

Mass (kDA):
152.241 kDA

Genomic Context

Human
Location:	3p21.31
Sequence:	3; NC_000003.12 (49886471..49903873, complement)

Tissue Specificity

Expressed in colon, skin, lung and bone marrow.

Subcellular Localizations

Membrane; Single-pass type I membrane protein.

Diseases

• Malignant Neoplasms
• Neoplasms
• Neoplasm Metastasis
• Malignant Neoplasm Of Breast
• Malignant Neoplasm Of Lung
• Cell Transformation, Neoplastic
• Stomach Neoplasms
• Carcinoma
• Ulcer
• Mammary Neoplasms
• Adenocarcinoma
• Malignant Paraganglionic Neoplasm

• Crohn Disease
• Tumor Progression
• Pulmonary Adenomatosis, Ovine
• Acute Erythroblastic Leukemia
• Colitis
• Lung Neoplasms

Interacting Proteins

• MST1
• PLXNB1
• PLXNB2
• PLXNB3

Pathways

• Cell Migration
• Pathogenesis
• Cell Growth
• Methylation
• Cell Proliferation
• Gastrulation
• Somitogenesis
• Proteolysis

• Angiogenesis
• Invasive Growth
• Rna Interference

PTMs

• Phosphorylation

• Methylation

Research Areas

• Apoptosis
• Cell Cycle and Replication
• GPCR
• Immune System Diseases
• Immunology

• Phospho-Specific
• Protein Kinase

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/MST1R

Best Uses Of The MST1R Marker From Boster Bio

The Boster Bio company was founded in 1993. They have been manufacturing antibodies and ELISA kits since 1993. Recently, they started offering PCR-related molecular biological products. They are committed to providing scientists with high quality products and have many services to help them. Boster Bio also provides technical support and resources for scientists to help them make the best of their products.

Picokine

LCRF0004 inhibits MST1R and decreases cell viability of MPM cells. The compound significantly reduced the viability of MPM cells at 48 h after treatment with 200 nM MST1. The cell cycle was not affected by inhibition of MST1. FACS was used as a tool to assess apoptosis. Picokine might be one of MST1R's best uses.

MST1R can be found in the MET protooncogene group. It is essential for the development of epithelial bone and neuro-endocrine tissue. It is essential for complete embryonic growth. It is a heterodimeric protein that has a transmembrane 150 kDa b chain. MST1R's phosphorylation during development is by MST1R and autophosphorylated via MST1.

In clinical settings, it is becoming more popular to use the MST1R mark in patients with malignant-pleural mesothelioma. Researchers are working to better understand the role of MST1R in malignant mesothelioma's pathogenesis. But how can you use this marker effectively?

MST1R can be activated in MPM patient cells and cell lines. It activates a subset phosphokinases that are involved in the ERK/AKT Signaling pathway. This suggests that MST1R may be a therapeutic target. The immune response is dominated by this receptor. Therefore, an increase in activity of MST1R in cancer cells may improve prognosis.

The MST1R gene has been identified as a nested PCR marker for detecting the presence of the MPM tumors. MST1 also appears to be higher in MPM patients than in benign. A study of MPM patients revealed that MST1 was overexpressed in both tumors and benign pleura. MST1 also overexpression was found in MPM tumors according to the Gordon MPM database. Also, the MPM patient database was analyzed using a Student two-sided t-test to assess differential gene expression. The results showed that MPM patients had significantly increased levels of all genes.

Three cell lines containing high levels of MST1R were tested for LCRF-0004. It was found to have a significant anti-proliferative action in the MPM cell line NCIH226 and the REN, but not in the normal mesothelial line LP9.

Picoband

The Picoband MST1R marker has been developed to detect the expression of MST1R in human tumors. This protein is encoded in the MST1R genes. It is a receptor for tyrosinekinase that may play a role in host defense. Intestinal, skin, and stomach cancers often harbor mutations in this gene. MST1R is altered in approximately 1.62% of cancers. MST1R gene changes are most often seen in cancers such as colon adenocarcinoma (cutaneous melanoma), lung adenocarcinoma (lung invasive duct carcinoma), and endometrioid-adenocarcinoma.

MST1R

The MST1R is a receptor with immunological relevance. It has been found that PBMCs from healthy individuals are significantly suppressed when stimulated with heat-killed M. avium plus IL-12 or IL-18. These findings suggest that MST1R -deficient cells could be susceptible to NTM. The MST1R-receptor is a cell target that can play an important part in the development of pNTM.

The MST1R genes have a functional relationship with FAK, c-MET, and FAK. The correlation between the two genes may be weak but still significant. The MST1R marker can be used for many purposes. It can be used in the identification of the gene of interest in patients with scoliosis/pNTMPEX. MST1R has been linked to cancer. Currently, there is no treatment for either scoliosis nor pNTMPEX.

Further, a low MST1R marker and high c-MET expression are associated with poorer prognosis. These findings are limited due to the fact that cluster 3 patients only represent a subset of the entire cohort. The study's sample size grew to a relatively small number when considering only stage II patients. This difference was most evident in stage I disease.

MST1R is involved with bone turnover. MST1R deficient mice are more at risk for osteoporosis. MST1R deficient mice can be protected with pharmacological inhibitors. A recent study on mice found that 13 of 21 patients had lower levels in plasma cleaved bone derived collagen. One-third had large drops that were clinically related to the Mayo Clinic's guidelines regarding the response to bone Antiresorptive Therapies. However, bone turnover is expected to increase with menopause.

Many types of cancer are caused by the MET receptor tyrosine kinase familial. c–MET and MST1R have close relationships. Their co-expression has been associated with poorer prognosis in multiple cancers. The expression of both MST1R and c-MET is a common characteristic in gastroesophageal cancer and has been associated with poor survival.

The MST1R marker can be associated with the activity FAK, which is a protein that plays a role in the development of many types of cancers. These three proteins can be correlated and have been independently associated with prognosis of stage II colorectal patients. These markers can be used to help doctors identify cancers by targeting upstream factors that are involved in the development of the disease. These results have implications for the early diagnosis of CRC using FAK and MST1R.