Thermo Fisher Scientific MerTK (Innate Immune Checkpoint) Monoclonal Antibody (MERTK/3023)
MERTK 단백질을 표적으로 하는 Mouse IgG2a 단일클론 항체로, 인간 시료에 반응합니다. IHC(P), IHC(PFA), Peptide Array 등 다양한 응용에 적합합니다. 단백질 A/G로 정제된 액상 항체이며, PBS(pH 7.4) 용액에 보존제를 포함하지 않습니다. 연구용으로만 사용 가능합니다.
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Applications and Tested Dilution
| Application | Tested Dilution | Publications |
|---|---|---|
| Immunohistochemistry (Paraffin) (IHC (P)) | Assay-dependent | - |
| Immunohistochemistry (PFA fixed) (IHC (PFA)) | 1–2 µg/mL | - |
| Peptide Array (Array) | Assay-dependent | - |
Product Specifications
| 항목 | 내용 |
|---|---|
| Species Reactivity | Human |
| Host / Isotype | Mouse / IgG2a |
| Class | Monoclonal |
| Type | Antibody |
| Clone | MERTK/3023 |
| Immunogen | Recombinant human MERTK protein fragment (around aa 55–148) |
| Conjugate | Unconjugated |
| Form | Liquid |
| Concentration | 1 mg/mL |
| Purification | Protein A/G |
| Storage Buffer | PBS, pH 7.4 |
| Contains | No preservative |
| Storage Conditions | -20°C, Avoid Freeze/Thaw Cycles |
| Shipping Conditions | Wet ice |
Target Information
MERTK (cMER) is a tyrosine kinase proto-oncogene involved in the retinal pigment epithelium (RPE) phagocytosis pathway, which is implicated in human retinal disease. It regulates various physiological processes including cell survival, migration, differentiation, and efferocytosis (phagocytosis of apoptotic cells).
Ligand binding induces autophosphorylation of MERTK, creating docking sites for downstream signaling molecules. Upon activation, it interacts with GRB2 or PLCG2 and triggers phosphorylation of MAPK1, MAPK2, FAK/PTK2, or RAC1. MERTK signaling contributes to macrophage clearance of apoptotic cells, platelet aggregation, cytoskeleton reorganization, and engulfment. In the RPE, it regulates phagocytosis of rod outer segment fragments. It also inhibits Toll-like receptor (TLR)-mediated innate immune responses by activating STAT1, leading to induction of SOCS1 and SOCS3.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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