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MERTK Antibody (N-term)

Purified Rabbit Polyclonal Antibody (Pab)

     
  • IHC-P - MERTK Antibody (N-term) AP7662a
    Formalin-fixed and paraffin-embedded human brain tissue reacted with MERK antibody (N-term), which was peroxidase-conjugated to the secondary antibody, followed by DAB staining. This data demonstrates the use of this antibody for immunohistochemistry; clinical relevance has not been evaluated.
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Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
IHC-P, E
Primary Accession Q12866
Reactivity Human
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Calculated MW 110249 Da
Antigen Region 21-51 aa
Additional Information
Gene ID 10461
Other Names Tyrosine-protein kinase Mer, Proto-oncogene c-Mer, Receptor tyrosine kinase MerTK, MERTK, MER
Target/Specificity This MERTK antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 21-51 amino acids from the N-terminal region of human MERTK.
Dilution IHC-P~~1:10~50
Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, followed by dialysis against PBS.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsMERTK Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name MERTK
Synonyms MER
Function Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to several ligands including LGALS3, TUB, TULP1 or GAS6. Regulates many physiological processes including cell survival, migration, differentiation, and phagocytosis of apoptotic cells (efferocytosis). Ligand binding at the cell surface induces autophosphorylation of MERTK on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with GRB2 or PLCG2 and induces phosphorylation of MAPK1, MAPK2, FAK/PTK2 or RAC1. MERTK signaling plays a role in various processes such as macrophage clearance of apoptotic cells, platelet aggregation, cytoskeleton reorganization and engulfment (PubMed:32640697). Functions in the retinal pigment epithelium (RPE) as a regulator of rod outer segments fragments phagocytosis. Also plays an important role in inhibition of Toll-like receptors (TLRs)-mediated innate immune response by activating STAT1, which selectively induces production of suppressors of cytokine signaling SOCS1 and SOCS3.
Cellular Location Cell membrane; Single-pass type I membrane protein
Tissue Location Not expressed in normal B- and T-lymphocytes but is expressed in numerous neoplastic B- and T-cell lines. Highly expressed in testis, ovary, prostate, lung, and kidney, with lower expression in spleen, small intestine, colon, and liver
Research Areas
Citations (0)
citation

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Background

Protein kinases are enzymes that transfer a phosphate group from a phosphate donor, generally the g phosphate of ATP, onto an acceptor amino acid in a substrate protein. By this basic mechanism, protein kinases mediate most of the signal transduction in eukaryotic cells, regulating cellular metabolism, transcription, cell cycle progression, cytoskeletal rearrangement and cell movement, apoptosis, and differentiation. With more than 500 gene products, the protein kinase family is one of the largest families of proteins in eukaryotes. The family has been classified in 8 major groups based on sequence comparison of their tyrosine (PTK) or serine/threonine (STK) kinase catalytic domains.

References

Thompson, D.A., et al., Am. J. Hum. Genet. 70(1):224-229 (2002).
Graham, D.K., et al., Cell Growth Differ. 5(6):647-657 (1994).
Weier, H.U., et al., Cytogenet. Cell Genet. 84 (1-2), 91-92 (1999).

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Discontinued
Cat# AP7662a
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