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AB151635

Recombinant Human TIM 3 protein

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Recombinant Human TIM 3 protein is a Human Fragment protein, in the 22 to 200 aa range, expressed in HEK 293 cells, with >95%, < 1 EU/µg endotoxin level, suitable for SDS-PAGE, HPLC.

View Alternative Names

CD366, TIM3, TIMD3, HAVCR2, Hepatitis A virus cellular receptor 2, HAVcr-2, T-cell immunoglobulin and mucin domain-containing protein 3, T-cell immunoglobulin mucin receptor 3, T-cell membrane protein 3, TIMD-3, TIM-3

Key facts

Purity

>95% SDS-PAGE

Endotoxin level

< 1 EU/µg

Expression system

HEK 293 cells

Tags

His tag C-Terminus

Applications

HPLC, SDS-PAGE

applications

Biologically active

No

Accession

Q8TDQ0

Animal free

No

Carrier free

No

Species

Human

Reconstitution

Reconstitute in PBS

Storage buffer

pH: 7.4 Constituents: 99% Phosphate Buffer, 0.88% Sodium chloride

storage-buffer

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Reactivity", "Dilution Info", "Notes"] }, "values": { "SDS-PAGE": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" }, "HPLC": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" } } }

Sequence info

[{"sequence":"SEVEYRAEVGQNAYLPCFYTPAAPGNLVPVCWGKGACPVFECGNVVLRTDERDVNYWTSRYWLNGDFRKGDVSLTIENVTLADSGIYCCRIQIPGIMNDEKFNLKLVIKPAKVTPAPTLQRDFTAAFPRMLTTRGHGPAETQTLGSLPDINLTQISTLANELRDSRLANDLRDSGATIRVDHHHHHH","proteinLength":"Fragment","predictedMolecularWeight":"20.9 kDa","actualMolecularWeight":null,"aminoAcidEnd":200,"aminoAcidStart":22,"nature":"Recombinant","expressionSystem":"HEK 293 cells","accessionNumber":"Q8TDQ0","tags":[{"tag":"His","terminus":"C-Terminus"}]}]

Properties and storage information

Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
-20°C
Appropriate long-term storage conditions
-20°C
Storage information
Avoid freeze / thaw cycle|Reconstitute for long term storage
False

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

TIM-3 also known as T cell immunoglobulin and mucin-domain containing-3 or HAVCR2 is a protein involved in immune regulation. It possesses an approximate mass of 35 kDa. TIM-3 is expressed on various immune cells including T cells NK cells and dendritic cells especially after activation. The expression level often changes in response to inflammatory conditions suggesting its role in modulating immune responses.
Biological function summary

TIM-3 functions as a checkpoint inhibitor impacting immune cell activity. It is not part of a larger physical complex but it modulates immune responses by interacting with its ligands such as Galectin-9 phosphatidylserine and CEACAM1. TIM-3 involvement in downregulating Th1 cell responses shows its necessary role in maintaining immune homeostasis. The protein also acts in regulating tolerance mechanisms and preventing autoimmunity.

Pathways

TIM-3 participation is seen in the immune checkpoint and T cell exhaustion pathways. TIM-3 signaling results in T cell inhibition affecting the PD-1 pathway as well. It shares a relationship with proteins like LAG-3 and PD-1 which are key to immune inhibitory signaling. These interactions depict TIM-3's role in immune tolerance during chronic infections and malignancies.

TIM-3 association with cancer and chronic infections provides insight into therapeutic implications. In cancer TIM-3 contributes to immune evasion often co-expressed with PD-1 leading to T cell exhaustion. In autoimmune diseases TIM-3 modulation may affect disease progression by influencing immune tolerance. Understanding TIM-3's role in these contexts aids in developing targeted therapies such as anti-TIM-3 antibodies to enhance immune responses in cancer while promoting tolerance in autoimmunity.

Specifications

Form

Lyophilized

Additional notes

ab151635 is more than 95% pure, as determined by SEC-HPLC and reducing SDS-PAGE. It is supplied as an 0.2 µm filtered solution.

General info

Function

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).

Sequence similarities

Belongs to the immunoglobulin superfamily. TIM family.

Post-translational modifications

O-glycosylated with core 1 or possibly core 8 glycans.. Phosphorylated on tyrosine residues; modestly increased after TCR/CD28 stimulation. Can be phosphorylated in the cytoplasmic domain by FYN (By similarity). Phosphorylation at Tyr-265 is increased by stimulation with ligand LGALS9.

Product protocols

Target data

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).
See full target information HAVCR2

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