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FCMR / FAIM3 Antibody (C-Terminus)

Rabbit Polyclonal Antibody

     
  • IHC - FCMR / FAIM3 Antibody (C-Terminus) ALS11681
    Anti-FAIM3 antibody IHC of human kidney.
    detail
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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
WB, IHC-P
Primary Accession O60667
Reactivity Human
Host Rabbit
Clonality Polyclonal
Calculated MW 43kDa
Dilution IHC-P (5 µg/ml), WB (1 µg/ml),
Additional Information
Gene ID 9214
Other Names Fas apoptotic inhibitory molecule 3, Regulator of Fas-induced apoptosis Toso, FAIM3, TOSO
Target/Specificity 13 amino acid peptide from near the carboxy terminus of human Toso
Reconstitution & Storage Short term 4°C, long term aliquot and store at -20°C, avoid freeze thaw cycles. Store undiluted.
PrecautionsFCMR / FAIM3 Antibody (C-Terminus) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name FCMR {ECO:0000303|PubMed:25888699, ECO:0000312|HGNC:HGNC:14315}
Function High-affinity Fc receptor for immunoglobulin M (IgM), both secreted and membrane-bound IgM (PubMed:19858324, PubMed:22675200, PubMed:36949194, PubMed:37095205). Primarily regulates IgM transport and homeostasis. Primarily regulates IgM transport and homeostasis. In lymphoid cells, enables exocytosis of membrane-bound IgM on the plasma membrane as well as endocytosis of IgM-antigen complexes toward lysosomes for degradation. In mucosal epithelium, mediates retrotranscytosis of antigen-IgM complexes across mucosal M cells toward antigen-presenting cells in mucosal lymphoid tissues (PubMed:21908732, PubMed:28230186). Triggers costimulatory signaling and mediates most of IgM effector functions involved in B cell development and primary immune response to infection. Likely limits tonic IgM BCR signaling to self-antigens for proper negative selection of autoreactive B cells in the bone marrow and for the maintenance of regulatory B cell pool in peripheral lymphoid organs. Mediates antibody responses to T cell-dependent and T cell-independent antigens and promotes induction of an efficient neutralizing IgG response. Engages in cross-talk with antigen-receptor signaling via the non-canonical NF- kappa-B, MAP kinases and calcium signaling pathways (PubMed:19858324, PubMed:22675200, PubMed:25601920, PubMed:30840890).
Cellular Location Cell membrane; Single-pass membrane protein. Early endosome membrane; Single-pass membrane protein. Golgi apparatus, trans- Golgi network membrane; Single-pass membrane protein. Lysosome membrane; Single-pass membrane protein. Note=Continuously recycles between cytoplasmic pool and the plasma membrane to bind as much IgM as possible
Tissue Location Expressed by CD19-positive B cells and CD4-positive and CD8-positive T cell populations in primary and secondary lymphoid tissues (at protein level). Among B cell subsets, detected in a subset of bone marrow pro- and pre-B cells, in most follicular and memory B cells and in a small subset of germinal center B cells (at protein level). Expressed at lower levels in CD56-positive NK cells (at protein level) (PubMed:19858324, PubMed:21908732, PubMed:22675200, PubMed:30840890). Expressed in lymph nodes, lung, thymus and kidneys Very weak expression detected in spleen, liver, heart, and salivary gland.
Research Areas
Citations (0)
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Background

May play a role in the immune system processes. Protects cells from FAS-, TNF alpha- and FADD-induced apoptosis without increasing expression of the inhibitors of apoptosis BCL2 and BCLXL. Seems to activate an inhibitory pathway that prevents CASP8 activation following FAS stimulation, rather than blocking apoptotic signals downstream. May inhibit FAS-induced apoptosis by preventing CASP8 processing through CFLAR up-regulation.

References

Hitoshi Y.,et al.Immunity 8:461-471(1998).
Li F.J.,et al.Blood 118:4902-4909(2011).
Kalnine N.,et al.Submitted (MAY-2003) to the EMBL/GenBank/DDBJ databases.
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Gregory S.G.,et al.Nature 441:315-321(2006).

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Discontinued
Cat# ALS11681
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