LIFR (leukemia inhibitory factor receptor) belongs to the family of cytokine receptors. LIFR forms a high-affinity receptor complex with gp130, which mediates the activity of LIF (leukemia inhibitory factor) and thus affects the differentiation, proliferation, and survival of a wide variety of cells in the adult and the embryo. Besides LIF, LIFR can also bind to and activate CNTF (ciliary neurotrophic factor) and CLC (cardiotrophin like cytokine). Evidence showed that in the retina, LIFR activating LIF, CT-1 and cardiotrophin like cytokine (CLC) are strongly upregulated in response to preconditioning with bright cyclic light leading to robust activation of signal transducer and activator of transcription-3 (STAT3) in a time-dependent manner. Further, blocking LIFR activation during preconditioning using a LIFR antagonist (LIF05) attenuated the induced STAT3 activation and also resulted in reduced preconditioning-induced protection of the retinal photoreceptors. These data demonstrate that LIFR and its ligands play an essential role in endogenous neuroprotective mechanisms triggered by preconditioning-induced stress. LIFR was newly found to be a suppressor of hepatocellular carcinoma (HCC), one of the world's top five causes of cancer-related deaths.
Human TNFSF14 Protein; also known as LIGHT; belongs to a member of the tumor necrosis factor (TNF) ligand family. It can bind to NFRSF3/LTBR. It is a ligand for TNFRSF14; which is a member of the tumor necrosis factor receptor superfamily; and it is also known as a herpesvirus entry mediator ligand (HVEML). TNFSF14 encodes a protein with a 37 aa cytoplasmic domain; 21aa transmembrane domain and 182 aa extracellular region. The gene is predominantly expressed in the spleen and also found in the brain. Weakly expressed in peripheral lymphoid tissues and in heart; placenta; liver; lung; appendix; and kidney; and no expression seen in fetal tissues; endocrine glands; or nonhematopoietic tumor lines. TNFSF14 protein was found to probably function as a costimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. Studies have shown that this protein can prevent tumor necrosis factor alpha mediated apoptosis in primary hepatocyte. Two alternatively spliced transcript variant encoding distinct isoforms have been reported.
LIGHT , also known as TNFSF14 or CD258 , is a newly identified member of the TNF superfamily (TNFSF14) that is expressed by activated T lymphocytes , monocytes , granulocytes , spleen cells , and immature dendritic cells. TNFSF14 / LIGHT / CD258 is a type II transmembrane protein that is known to bind 2 membrane-bound TNFSF signaling receptors: HVEM , which is predominantly expressed by T cells , and lymphotoxin β receptor (LTβR) , which is expressed by stromal cells and nonlymphoid hematopoietic cells. TNFSF14 / LIGHT / CD258 also binds to a soluble non-signaling receptor , decoy receptor 3 (DcR3) , which can modulate the function of LIGHT in vivo. TNFSF14 / LIGHT / CD258 can also costimulate T cell responses via HVEM , which is constitutively expressed in most lymphocyte subpopulations , including CD4+ and CD8+ T cells. In addition , TNFSF14 / LIGHT / CD258 has been shown to suppress tumor formation in vivo and to induce tumor cell apoptosis via the up-regulation of intercellular adhesion molecule 1 and an increased lymphocyte adhesion to cancer cells. Thus , TNFSF14 / LIGHT / CD258 is being actively investigated as a possible basis for cancer treatment.
May act as receptor for class I MHC antigens.
Leukocyte Immunoglobulin-Like Receptor Subfamily A Member 2 (LILRA2) is a single-pass type I membrane protein. LILRA2 is expressed predominantly on monocytes and B cells, and at lower levels on dendritic cells and natural killer cells. LILRA2 contains four Ig-like C2-type domains, with short cytoplasmic domains lacking an immunoreceptor tyrosine-based inhibitory motif (ITIM) and with transmembrane regions containing a charged arginine residue, may initiate stimulatory cascades. LILRA2 does not bind class I MHC antigens.
Inserisci la tua e-mail e seleziona le aree di interesse per ricevere le ultime novità, approfondimenti e promozioni.
Seleziona uno o più ambiti di interesse per ricevere comunicazioni più utili e mirate.
2025 TEMA Ricerca - All Rights Reserved.
