FAIM3

Official Full Name

Fc mu receptor

Organism

Homo sapiens

GeneID

9214

Background

Fc receptors specifically bind to the Fc region of immunoglobulins (Igs) to mediate the unique functions of each Ig class. FAIM3 encodes an Fc receptor for IgM (see MIM 147020) (Kubagawa et al., 2009 [PubMed 19858324]; Shima et al., 2010 [PubMed 20042454]).[supplied by OMIM, Jul 2010]

Synonyms

FCMR; TOSO; FAIM3; FcmuR; IgM FcR;

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Detailed Information

Human FAIM3 (also known as FCMR or TOSO) gene is located in the q13.12 zone of chromosome, which is highly expressed in digestive and urinary tracts, bone marrow and testes, and restricted to cerebellum in the nervous system according to the human protein atlas data. In the perspective of its own structure, FAIM3 is a transmembrane protein belonging to the Immunoglobulin family owing to the containing of Immunoglobulin-like domain for the binding with IgMs, which is necessary for the anti-apoptotic functionality of this protein. It is reported FAIM3 can protect Jurkat cell from FasL or TNFα induced apoptosis but not TNF-related apoptosis-inducing ligand.

FAIM3 presents 2 different mechanisms for the protection on the DR induced apoptosis, one is inducing DR antagonist CFLAR (also called CFLIP) to compete with caspase-8 blocking the activation of initiator caspases at DISC, and later Song's research revealed FAIM3s interaction with FADD, thus further confirmed the disruption of DISC's formation may be the mechanism. Another is Lee's hypothesis that FAIM3 protection depended on RIPK1 ubiquitination and recruitment of the death FADD to a TOSO/RIPI protein complex. RIPK1 is serine threonine kinase responsible for inflammation and apoptosis signaling transmission following DR activation. Then FAIM3 elevates the proportion of pro-survival signaling through MAPK/ERK and NF-jB pathway after DR activation. FAIM3 null mouse generated by homologous recombination revealed FAIM3 participation in the activation of innate immune system in response to bacterial infection. Beyond this, the granulocytes of FAIM3-deficient mice presented a deregulated state of reactive oxygen species and cytokine formation and impaired phagocytic capacity.

FAIM3 overexpression has been proven to be progressed closely with lymphocytic leukemia in the context of cancer research. Highly-expressed FAIM3 may be a specific characterization of chronic lymphocytic leukemia cells while not other B-cell lymphomas types according to protein and mRNA expression analysis. However, functionality and outcome of this high expression has not been clarified. FAIM3 shown a link with activation and homeostasis of innate immune system. In particular, Sigruener's observation manifested the resistance to the development of experimental autoimmune encephalomyelitis (EAE) of FAIM3-deficient mice. More and more evidence supports that neurodegenerative disease is associated with immune monitoring system, which is responsible for controlling the responses to threatening signals according to their duration and magnitude. And it will trigger an inflammatory reaction including not only programmed cell death of primary cell but also leakage of the dead cell content induced adjacent sensitized cell death to deteriorate the tissue. Shading from inflammatory disease via blocking FAIM3 may easily lead to the hypothesis that this therapy strategy is beneficial for inflammation featured neurodegenerative disease.

Anti-Faim-3 Monoclonal Antibody in Clinical Trials

Blocking antibody for anti-FAIM3 progressed well in pre-clinical EAE model is reported by Brenner and its collaborator. Different species of anti-FAIM3 monoclonal antibody generated by Nguyen group is considered to be used in clinical trials. Those anti-FAIM3 based modulators for DRs dysregulation would set off a new beginning in the therapeutic strategies for neurodegenerative disease.

Fig 1. Proposed mechanism of FAIM action in B-cells (Mitelman et al. 2009)

References:

Laura Planells-Ferrer, Jorge Urresti. (2016) 'Fas apoptosis inhibitory molecules: more than death-receptor antagonists in the nervous system, Journal of Neurochemistry, doi: 10.1111/jnc.13729.
Murakami Y. Narayanan S. Su S. Childs R. (2012) 'a functional IgM receptor, is regulated by IL-2 in T and NK cells, J. Immunol, 189, 587–597.
Miguel F Segura, Carme Sole, Rana S Moubarak. (2009) 'FAIM (Fas apoptotic inhibitory molecule). Atlas of Genetics and cyrogenetics in oncology and haematology.

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