HAVCR2: A TIM Family Protein with Potential Drug Targeting and Biomarkering

Target Name: HAVCR2

NCBI ID: G84868

HAVCR2: A TIM Family Protein with Potential Drug Targeting and Biomarkering

HAVCR2 (TIM-3) is a protein that is expressed in various tissues throughout the body, including the skin, hair, and nails. It is a member of the TIM family of proteins, which are known for their role in cell signaling and division. HAVCR2 has been identified as a potential drug target and biomarker for various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders.

The TIM family of proteins were first identified in the 1990s as key regulators of cell signaling pathways. The TIM family consists of four subunits: TIM-1, TIM-2, TIM-3, and TIR. All of these subunits have a characteristic alpha-helical structure and a catalytic active site that is involved in the regulation of protein-protein interactions and the dynamics of cells.

HAVCR2 is a 21-kDa protein that is expressed in various tissues, including the skin, hair, and nails. It is a member of the TIM family and is involved in the regulation of cell signaling pathways. HAVCR2 has been shown to play a role in the development and progression of various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders.

One of the key functions of HAVCR2 is its role in the regulation of cell adhesion. Adhesion is the process by which cells stick together to form tissues and organs. HAVCR2 is involved in the regulation of cell adhesion by controlling the interactions between cells and the extracellular matrix (ECM). This is important for the development and maintenance of tissues and organs, as well as for the regulation of embryonic development.

In addition to its role in cell adhesion, HAVCR2 is also involved in the regulation of cell proliferation and apoptosis. Proliferation is the process by which cells divide, and apoptosis is the process by which cells die. HAVCR2 is involved in the regulation of cell proliferation by controlling the production of factors that promote cell growth and the inhibition of factors that promote cell cycle arrest. In addition, HAVCR2 is also involved in the regulation of cell apoptosis by controlling the production of factors that promote apoptosis and the inhibition of factors that prevent apoptosis.

HAVCR2 has also been shown to be involved in the regulation of immune responses. The immune system is important for protecting the body against infection and disease, and HAVCR2 is involved in the regulation of the immune response by controlling the interactions between immune cells and the ECM. This is important for the regulation of autoimmune diseases, in which the immune system attacks the body's own tissues.

In conclusion, HAVCR2 is a protein that is involved in the regulation of cell signaling pathways and the development and progression of various diseases. As a potential drug target and biomarker, HAVCR2 is a promising target for the development of new treatments for a variety of diseases. Further research is needed to fully understand the role of HAVCR2 in cell signaling and the development and progression of diseases.

Protein Name: Hepatitis A Virus Cellular Receptor 2

Functions: Cell surface receptor implicated in modulating innate and adaptive immune responses. Generally accepted to have an inhibiting function. Reports on stimulating functions suggest that the activity may be influenced by the cellular context and/or the respective ligand (PubMed:24825777). Regulates macrophage activation (PubMed:11823861). Inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses and promotes immunological tolerance (PubMed:14556005). In CD8+ cells attenuates TCR-induced signaling, specifically by blocking NF-kappaB and NFAT promoter activities resulting in the loss of IL-2 secretion. The function may implicate its association with LCK proposed to impair phosphorylation of TCR subunits, and/or LGALS9-dependent recruitment of PTPRC to the immunological synapse (PubMed:24337741, PubMed:26492563). In contrast, shown to activate TCR-induced signaling in T-cells probably implicating ZAP70, LCP2, LCK and FYN (By similarity). Expressed on Treg cells can inhibit Th17 cell responses (PubMed:24838857). Receptor for LGALS9 (PubMed:16286920, PubMed:24337741). Binding to LGALS9 is believed to result in suppression of T-cell responses; the resulting apoptosis of antigen-specific cells may implicate HAVCR2 phosphorylation and disruption of its association with BAG6. Binding to LGALS9 is proposed to be involved in innate immune response to intracellular pathogens. Expressed on Th1 cells interacts with LGALS9 expressed on Mycobacterium tuberculosis-infected macrophages to stimulate antibactericidal activity including IL-1 beta secretion and to restrict intracellular bacterial growth (By similarity). However, the function as receptor for LGALS9 has been challenged (PubMed:23555261). Also reported to enhance CD8+ T-cell responses to an acute infection such as by Listeria monocytogenes (By similarity). Receptor for phosphatidylserine (PtSer); PtSer-binding is calcium-dependent. May recognize PtSer on apoptotic cells leading to their phagocytosis. Mediates the engulfment of apoptotic cells by dendritic cells. Expressed on T-cells, promotes conjugation but not engulfment of apoptotic cells. Expressed on dendritic cells (DCs) positively regulates innate immune response and in synergy with Toll-like receptors promotes secretion of TNF-alpha. In tumor-imfiltrating DCs suppresses nucleic acid-mediated innate immune repsonse by interaction with HMGB1 and interfering with nucleic acid-sensing and trafficking of nucleid acids to endosomes (By similarity). Expressed on natural killer (NK) cells acts as a coreceptor to enhance IFN-gamma production in response to LGALS9 (PubMed:22323453). In contrast, shown to suppress NK cell-mediated cytotoxicity (PubMed:22383801). Negatively regulates NK cell function in LPS-induced endotoxic shock (By similarity)

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