MST1 Antibodies

Hepatocyte growth factor-like protein (MST1)

Gene Information

Human
Gene Name:	MST1
Uniprot:	P26927
Entrez:	4485

Family

Belongs to:
peptidase S1 family

Alternative Names

D3F15S2; EC 3.4.21; hepatocyte growth factor-like protein homolog; HGFL; HGFLhepatocyte growth factor-like protein; macrophage stimulating 1 (hepatocyte growth factor-like); Macrophage stimulatory protein; Macrophage-stimulating protein; MSP; MSPDNF15S2; MST1; NF15S2; SF2

Molecular Weight

Mass (kDA):
80.32 kDA

Genomic Context

Human
Location:	3p21.31
Sequence:	3; NC_000003.12 (49683947..49689523, complement)

Subcellular Localizations

Secreted.

Diseases

• Neoplasms
• Malignant Neoplasms
• Cell Transformation, Neoplastic
• Crohn Disease
• Carcinoma
• Ulcer
• Tissue Adhesions
• Colitis
• Common Wart
• Inflammatory Bowel Diseases
• Ulcerative Colitis
• Neoplasm Metastasis
• Colorectal Cancer

• Intestinal Diseases
• Liver Carcinoma
• Colorectal Neoplasms
• Cell Invasion
• Hypertrophy
• Hyperplasia
• Liver Neoplasms

Interacting Proteins

• MST1R
• STK11

Pathways

• Cell Death
• Cell Proliferation
• Cell Cycle
• Cell Growth
• Localization
• Methylation
• Induction Of Apoptosis
• Pathogenesis
• Rna Interference
• Cell Adhesion
• Histone Modification
• Transport
• Dna Methylation

• Translation
• Chromosome Segregation
• Centrosome Duplication
• Organ Development
• Programmed Cell Death
• Chemotaxis
• Angiogenesis

PTMs

• Phosphorylation
• Cleavage
• Methylation
• Acetylation
• Dephosphorylation
• Myristoylation

• Glutathionylation
• Acylation
• Ribosylation
• Ubiquitination
• Reduction
• Deacetylation

• Oxidation

Research Areas

• Protein Kinase

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/MST1

Best Uses Of The MST1 Marker

MST1 is a possible therapeutic target. It regulates cell trafficking and naive T cells homeostasis. In addition, it regulates activity of FoxO1 and FoxO3 transcription factors. MST1 also regulates cellular oxidative stress. It is, in the end, an essential regulatory protein in T cell homeostasis. However there are some limitations to its application.

MST1 could be a therapeutic target

In this study, we demonstrate that MST1 suppresses the viability of glioma cells by upregulating SIRT6. In glioma cell lines, we also observed that SIRT6 and MST1 expression is positively correlated. In addition, we show that MST1 can inhibit cell proliferation, as revealed by the MTT assay. Therefore, MST1 could be a novel therapeutic target for Boster Bio.

MST1 could be a promising therapeutic target because it inhibits the cleavage-based apoptosis process in the glioblastoma multiform. Boster bio's antiapoptotic drug MST1 further supports its effects.

In the beginning, we wanted to understand the molecular basis behind MST1 the kinase's activation in Glioma cells. We identified the mutation through co-transfection of GST with Myc-tagged MST1 constructs. We then conducted GST pulldown assays to analyze the interaction between MST1 and UNC5B. We also discovered that kinase-dead UNC5B had a weaker relationship with MST1. Additionally, the irresistible D412N mutant showed strong binding activity towards MST1. Additionally, T428E exhibited a stronger interaction than WT UNC5B . However, T428A did not show any interaction with MST1.

The mechanisms that govern the Hippo pathway are not fully understood. However, we have found that MST1 activates the UNC5B receptor and reduces the activity of NTN1, which is the main cause of dopaminergic neuronal death in PD. MST1 also phosphorylates the UNC5B receptor at the T428 residue and inhibiting UNC5B causes neuronal death.

We found that blocking UNC5B phosphorylation reduced the activity of caspase-3, a molecule accountable for the oxidative stress in cells. Additionally, our results revealed that MST1 inhibited the levels of TH and total YAP in PD patients. Genetic knockdown of this protein prevented neuronal deaths from ICH. So, we found that MST1 was a potential therapeutic target for Boster Bio.

The company's research focuses on finding drugs that target MST1. The scientists dissect postmortem brain tissue and infect HEK 293 cells with plasmids to create new cell lines. This process is called cell fusion and this research could prove very beneficial in treating Alzheimer's Disease as well as other neurodegenerative disorders. Boster Bio is also interested in this therapeutic target because it targets MST1 to be a possible treatment for cancer.

Boster Bio is focusing on the mst1 genesthat are involved in SIRT6 expression. By reducing MST1, it may aid in treating glioma and other tumors. In addition, MST1 also positively regulates SIRT6 expression, a biomarker for the presence of glioma. This protein is therefore an ideal target for Boster Bio's antiangiogenic drugs.

The team also tested the effects of a virus known as Tat-DCC-4Fbn on the motor function of mice. They used two or three-month-old mice as test subjects. Each mouse was anesthetized isoflurane and injected with meloxicam (5 mg/kg) subcutaneously. The rotarod test was utilized to monitor each mouse for motor impairment.

It regulates cell phone trafficking

The MST1 marker, which is a molecular determinant for cell-trafficking is multifunctional. Its role in the control of cell trafficking might be due to its relationship with IRAK1. MST1 inhibits the pro-inflammatory response and promotes the production of IFN-b. It could also function as a substrate for IRAK1.

The MST1 receptor is a component of the Toll receptor and is a well-known regulator of apoptosis. MST1 was first identified in an Drosophila test for tumor suppressor genes. The absence of MST1 causes a form of hepatocellular cancer and intestinal epithelium-specific tumors. Thus, MST1 may play a part in limiting the oncogenic capacity of tumor cells in mammals.

The MST1 receptor binds to GA and allows cytosolic transport. Its activation can be triggered by the increase in H2O2. Inactivation of Prdx1 enforces this feedback mechanism, extending Mst1's activity and resulting in increased levels of oxidants and DNA damage. Thus, MST1/2 could act as tumor suppressors, preventing the accumulation of mutations.

Besides T cells, MST1 can also be expressed in other cells of the hematopoietic system. MST1 could regulate LPL during B-cell trafficking. The amino acid sequence around Thr 89 is conserved across nonhematopoietic forms of plastin including T-plastin. T-plastin promotes axonogenesis and I-plastin, which helps maintain microvilli as well as the epithelia barrier.

MST1 is vital for normal vasculature development. MST2 is also essential for proper functioning of the primary hemopoiesis. In addition, the mice that had MST1 showed significant growth retardation. They also showed impaired placental development and hematopoiesis that was primitive, as well as reduced growth of the placenta. MST1 and MST2 are therefore crucial for the early development of mice.

Drosophila's Hippo pathway is crucial for epithelial growth and differentiation. In mammals, Mst kinases may play roles in different pathways. Spatial and temporal regulation can influence Mst signaling components and substrate specificity during embryogenesis. The MST1 marker is essential for the early development. MST1 plays a role in many physiological processes, including the regulation of Mst signaling.

MST Kinases are emerging as important regulators of the immune system. They regulate the inborn immune response by regulating the activity of signal molecules through direct phosphorylation. This paper outlines the function and recent developments in MST kinases' roles in regulation in the innate immune response. You are more susceptible to infections and have a less immune response when you have MST1 deficiencies.

In mice, MST1 dissociates from trx-1 and activates the MST1 gene. Mutant SOD1 inhibits apoptosis by targeting FOXO. The downstream targets of Mst1's are FOXO3 & FOXO1.

It controls Ag receptor-induced activation of naive T cells

The TCR is an important part of the immune system, as it is responsible for the majority of immune responses. The antigen-specific T cells in the body exchange signals with one another and orchestrate immune responses to foreign antigens. But for T cells that are not naive to become activated, they must first receive several different signals. The antigen itself is created by the TCR engagement. In addition, a range of co-stimulatory molecules are also necessary to activate T cells. Resting antigen-presenting cells do not usually express enough co-stimulatory proteins to activate T cells.

We investigated the function of the TCR in the naive T cells by looking at the phosphorylation levels of several molecules on T-cells. OVAp induced the phosphorylation CD3z and ZAP70 within macrophages but only to a small extent. Contrarily the OVAp that is soluble OVAp loaded macrophages caused Y315 and Y132 phosphorylation of LAT.

Another immune system cell that recognizes pathogen associated molecular patterns (PAMPs), is the Toll-like family of receptors. When these molecules are analysed and analyzed, they result in rapid recruitment of more cells and an immediate increase in the inflammatory process. In inflammatory conditions, phagocytes, tissue dendritic and tissue cells remove damaged tissue, migrate into lymph nodes and release peptides to T cells.

In this study, we used the surrogate marker 5-ethynyl-2'-deoxyuridine (EDU) to detect T cell proliferation. CD19-DARIC T cell proliferation levels were comparable in the absence of dimerization agents, however, they showed little uptake of EdU. This is because the DARIC signaling structure shows lower basal activity and gains the ability to signal when dimerizing agents are present.

CD137 is part of the TNF receptor family. It binds with the CD137 ligand (also called CD137L). Costimulatory molecules also are produced by the antigen-presenting cell, which are utilized to activate T cells. This ligand is vital for T-cell differentiation and clonal expansion. These costimulatory molecules also stimulate naive CD4+ T cells.

In this study, IL-2 mediated FOXP3 expression was significantly diminished in nTregs with CD4+CD25hi that were stimulated TGFb mAbs that were anti-tGFb. TGFb1 did not influence FOXP3 expression in cells that had CD4+CD25hi nucleated although it was higher than cells that were not stimulated.

The signaling cascade that triggers TCR and CD28 through the CD28/CTLA-4 pathway is assisted by the CD28/CTLA-4 pathway. By doing this cells are able keep its activation cascade running long enough to encourage proper proliferation, effector differentiation, and memory cells. CD28 does not have the capacity to activate CD4+ T cells. However, it regulates T cell signaling.