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> MHC class I polypeptide-related sequence B (MICB) MHC class I polypeptide-related sequence B (MICB)
MICB seems to have no role in antigen presentation. MICB acts as a stress-induced self-antigen that is recognized by gamma delta T cells. Ligand for the KLRK1/NKG2D receptor. Binding to KLRK1 leads to cell lysis.
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MHC class I polypeptide-related sequence B (MICB) Related Products
MICB Proteins
- Human MICB/Fc Protein, Recombinant, Cat NO: 10759-H03H
- Human MICB Protein. Recombinant, Cat NO: 10759-H08H
MICB Antibodies
- Anti-Human MICB Antibody, Mouse MAb, Cat NO: 10759-MM09
- Anti-Human MICB Antibody, Mouse MAb, Cat NO: 10759-MM12
- Anti-Human MICB/MIC-B Antibody (FITC), Cat NO: 10759-MM12-F
- Anti-Human MICB Antibody, Rabbit MAb, Cat NO: 10759-R103
- Anti-Human MICB Antibody, Rabbit PAb, Cat NO: 10759-RP01
- Anti-Human MICB Antibody, Rabbit PAb (Antigen Affinity Purified), Cat NO: 10759-RP02
MICB ELISA Pair sets
MICB cDNA Clones
MHC class I polypeptide-related sequence B (MICB) Related Areas
Immunology>>Adaptive Immunity>>Major Histocompatibility Complex>>MICB
MHC class I polypeptide-related sequence B (MICB) Related Pathways
MHC class I polypeptide-related sequence B (MICB) Alternative Names
MICB, DAAP-210H10.1, PERB11.2
Summaries for MHC class I polypeptide-related sequence B (MICB)
Entrez Gene summary for MICB:
This MICB gene encodes a heavily glycosylated protein which is a ligand for the NKG2D type II receptor. Binding of the ligand activates the cytolytic response of natural killer (NK) cells, CD8 alphabeta T cells, and gammadelta T cells which express the receptor. MICB is stress-induced and is similar to MHC class I molecules; however, it does not associate with beta-2-microglobulin or bind peptides. [provided by RefSeq, Jul 2008]
Wikipedia summary for MICB:
MHC class I polypeptide-related sequence B is a protein that in humans is encoded by the MICB gene.
Human MHC class I polypeptide-related sequence B (MICB) Protein General Information
| Protein names |
MHC class I polypeptide-related sequence B, Short name=MIC-B |
| Sequence length |
383 AA. |
| Induction |
By heat shock, oxidative stress, retinoic acid, IFN-alpha and the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine. Induction by IFN-alpha is impaired in patients with chronic hepatitis C virus infection. MICB is down-regulated by human cytomegalovirus UL112 microRNA during viral infection which leads to decreased binding of KLRK1/NKG2D and reduced killing by natural killer cells. |
| Sequence similarities: |
MICB belongs to the MHC class I family. MIC subfamily. MICB contains 1 Ig-like C1-type (immunoglobulin-like) domain. |
| Polymorphism: |
The following alleles of MICB are known: MICB*001, MICB*002, MICB*003, MICB*004, MICB*005, MICB*006, MICB*007, MICB*008, MICB*009N, MICB*010, MICB*011, MICB*012, MICB*013, MICB*014, MICB*015, MICB*016, MICB*018, MICB*019, MICB*020, MICB*021N and MICB*022. MICB*009N and MICB*021N are null alleles which are not expressed. The sequence shown is that of MICB*001. |
| Post-translational modification: |
Proteolytically cleaved and released from the cell surface of tumor cells. |
| Subunit structure |
Unlike classical MHC class I molecules, does not form a heterodimer with beta-2-microglobulin. MICB binds as a monomer to a KLRK1/NKG2D homodimer. KLRK1 forms a complex with HCST/DAP10 in which KLRK1 binds MICB while HCST acts as an adapter molecule which enables signal transduction. Receptor-ligand interaction induces clustering of both proteins in ordered structures called immune synapses and also leads to their intercellular transfer. This is associated with a reduction in the cytotoxicity of KLRK1-expressing cells. MICB binds to human cytomegalovirus glycoprotein UL16 which causes sequestration of MICB in the endoplasmic reticulum and increases resistance to KLRK1-mediated cytotoxicity. |
| Subcellular location: | Cell membrane; Single-pass type I membrane protein By similarity. Note: Binding to human cytomegalovirus glycoprotein UL16 causes sequestration in the endoplasmic reticulum. |
| Tissue specificity |
MICB is widely expressed with the exception of the central nervous system where it is absent. MICB is expressed in many, but not all, epithelial tumors of lung, breast, kidney, ovary, prostate and colon. In hepatocellular carcinomas, expressed in tumor cells but not in surrounding non-cancerous tissue. |
| Involvement in disease: | Genetic variations in MICA are a cause of susceptibility to rheumatoid arthritis (RA) [MIM:180300]. It is a systemic inflammatory disease with autoimmune features and a complex genetic component. It primarily affects the joints and is characterized by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Note=The MICB*004 allele is associated with rheumatoid arthritis. Note=Genetic variation in MICB is associated with cytomegalovirus and herpes simplex virus I seropositivity and this may be associated with schizophrenia risk. |
General information above from UniProt
Function for MHC class I polypeptide-related sequence B (MICB) Protein
UniProtKB:
MICB seems to have no role in antigen presentation. MICB acts as a stress-induced self-antigen that is recognized by gamma delta T cells. Ligand for the KLRK1/NKG2D receptor. Binding to KLRK1 leads to cell lysis.
Genatlas:
- MICB is involved in the presentation of foreign antigens to the immune system
- MICA, and MICB, ligands of the KLRK1, which activates NK cells and costimulates effector T cells, are inducibly expressed under harmful conditions, such as malignancies and microbial infections (Pubmed 17202358)

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