Recombinant Human Hepatitis A virus cellular receptor 2(HAVCR2),partial

Code CSB-YP010145HU
Size US$250
  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
Have Questions? Leave a Message or Start an on-line Chat

Product Details

Greater than 90% as determined by SDS-PAGE.
Target Names
Uniprot No.
Research Area
Alternative Names
CD366; FLJ14428; HAVcr-2; Havcr2; HAVR2_HUMAN; Hepatitis A virus cellular receptor 2; Kidney injury molecule 3 ; KIM 3; KIM3; T cell immunoglobulin and mucin domain containing 3; T cell immunoglobulin mucin 3; T-cell immunoglobulin and mucin domain-containing protein 3; T-cell immunoglobulin mucin family member 3; T-cell immunoglobulin mucin receptor 3; T-cell membrane protein 3; Tim 3; TIM-3; TIM3; TIMD-3; TIMD3
Homo sapiens (Human)
Expression Region
Target Protein Sequence
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
Protein Length
Extracellular Domain
Tag Info
N-terminal 6xHis-tagged
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.

Presenting our high-quality Recombinant Human HAVCR2, an ideal research tool for investigators in the field of immunology. Hepatitis A virus cellular receptor 2 is a membrane glycoprotein implicated in the regulation of immune responses and has garnered attention for its potential therapeutic applications. Our recombinant protein offers exceptional performance to support your experimental needs with confidence and reliability.

Recombinant Human HAVCR2 is expressed in yeast, encompassing the extracellular domain of the protein, spanning the expression region from 22-202 amino acids. The protein is N-terminal 6xHis-tagged, facilitating ease of purification and detection. With a purity greater than 90% as determined by SDS-PAGE, this product ensures consistent performance and excellent quality for your research endeavors. Recombinant Human HAVCR2 is available in both liquid and lyophilized powder forms to accommodate your specific research requirements.

Customer Reviews and Q&A

 Customer Reviews

There are currently no reviews for this product.

Submit a Review here

Target Background

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. Regulates macrophage activation. Inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses and promotes immunological tolerance. 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. In contrast, shown to activate TCR-induced signaling in T-cells probably implicating ZAP70, LCP2, LCK and FYN. Expressed on Treg cells can inhibit Th17 cell responses. Receptor for LGALS9. 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. However, the function as receptor for LGALS9 has been challenged. Also reported to enhance CD8+ T-cell responses to an acute infection such as by Listeria monocytogenes. 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. Expressed on natural killer (NK) cells acts as a coreceptor to enhance IFN-gamma production in response to LGALS9. In contrast, shown to suppress NK cell-mediated cytotoxicity. Negatively regulates NK cell function in LPS-induced endotoxic shock.
Gene References into Functions
  1. TIM-3 expression was predominantly localized to myeloid cells in both human and murine tumors PMID: 29316433
  2. TIM-3 and IL-37 may be used as potential biomarkers of active rheumatoid arthritis. PMID: 30106887
  3. High TIM3 expression is associated with gastric cancer. PMID: 30106451
  4. miR-498 can effectively suppress TIM-3 expression in the acute myeloid leukemia cell line PMID: 30107988
  5. These results indicate that TIM-3 may be involved in the pathogenesis of immune thrombocytopenia which subsequently can represent an opportunity for new therapeutic plan, moreover. This may have a prognostic value for disease severity. PMID: 28974109
  6. Within many tumors, PD-1/Tim-3 coexpressing CD8-T cells lose their ability to secrete cytokines and their intratumoral infiltration correlates with a bad prognosis. Tim-3 appeared as a potential biomarker of anti-PD-1 resistance. Combined blockade of PD-1 and Tim-3 axis demonstrated potent clinical efficacy in preclinical models and reinforced the rationale of using an anti-Tim-3 to override tumor resistance.[review] PMID: 29547109
  7. this study shows that TIM-3 expression identifies a distinctive PD-1(+) follicular helper T cell subset, with reduced interleukin 21 production and B cell help function in ovarian cancer patients PMID: 29482158
  8. TIM-3 high expression rate was an independent prognostic factor for extranodal NK/T cell lymphoma, nasal type PMID: 28901003
  9. sTim-3 is a promising biomarker for allograft dysfunction, but unable to differentiate allograft rejection from other causes of renal dysfunction in kidney transplantation recipients PMID: 29310109
  10. The expression of Tim-3 on CD14+ monocytes is involved in systemic inflammatory reaction after intracerebral hemorrhage. PMID: 29310959
  11. TIM-3 gene may play an important role as a genetic risk factor for the progression and prognosis of invasive breast cancer. PMID: 29263040
  12. Tim-3(+) NK cells had decreased capability of IFN-r secretion, while Tim-3(+) monocytes showed a M2-like phenotype. Importantly, Tim-3 level on both NK cells and monocytes positively correlated with the ratio of Ki-67(+) tumor cells. PMID: 29174343
  13. T-cell immunoglobulin mucin-3/galectin-9 (Tim-3/Gal-9) binding signaling can also engage other binding partners to induce distinct cellular responses [Review]. PMID: 29027155
  14. Polymorphism +4259A>C in exon 3 of the TIM-3 gene is associated with susceptibility to multiple sclerosis but polymorphism -1637C>T in the promoter region of TIM-1 is not. PMID: 29141799
  15. The interaction between Gal-9/TIM-3 pathway and follicular helper cells contributed to viral persistent in chronic hepatitis C virus infection. PMID: 28772217
  16. Exosomal total protein, Tim-3 and Galectin-9 were up-regulated in non-small cell lung cancer plasma. PMID: 29452091
  17. the monitoring of sTim3 in urine may be a novel and promising noninvasive approach for the detection of AR. Furthermore, measurement of sTim3 in urine may contribute to predict the response to antirejection therapy and a poor outcome following AR. PMID: 28586044
  18. the CD4(+)CD25(+)Foxp3(+) Treg cells from RA patients demonstrated a reduction of Tim3 and were less functional than Treg cells from healthy controls in a Tim3-related manner. PMID: 28478516
  19. our study highlights the role of TIM-3 as a potential prognostic marker and a promising therapeutic target in solid tumors. PMID: 28423646
  20. HAVCR2 regulates cytokines, chemokines, prostaglandins and cell adhesion molecules in the presence of viral infection, which suggests a potential for HAVCR2 activators as therapeutics for the management of preterm birth associated with viral infections. PMID: 28466996
  21. serum levels may be increased in patients with early phase diffuse cutaneous systemic sclerosis and associated with cardiac involvement and renal crisis PMID: 27651303
  22. Preoperative Tim3 expression on peripheral NK cells is correlated with differential staging in colorectal cancer, and may be useful as a serum biomarker. PMID: 28440449
  23. TIM-3 polymorphism is associated with response to therapy in hepatitis B virus-related hepatocellular carcinoma. PMID: 27034168
  24. BMI-1, TIM-3 and CLL-1 have roles in acute myeloid leukemia prognosis and therapy PMID: 27506934
  25. Quantification of TIM-3 and KIM-1 mRNA expressions, along with KIM-1 protein measurements in urine and blood could be employed as promising tools for noninvasive diagnosis of allograft dysfunction. PMID: 28757398
  26. Results show that human acute myeloid leukemia (AML) cells possess a secretory pathway which leads to the production and release of soluble Tim-3 and galectin-9. Both proteins prevent the activation of NK cells and impair their AML cell-killing activity. PMID: 28750861
  27. after 14 days of glucocorticoid therapy, clinical findings (serum bilirubin, skin GVHD) and plasma biomarkers (TIM3, ST2, sTNFR1) can predict failure of GVHD treatment and nonrelapse mortality. PMID: 28478120
  28. These findings suggested that rs10053538 in TIM-3 might increase susceptibility to and promote the progression of breast cancer in Chinese women PMID: 27248321
  29. Results indicate that T cell Ig and mucin domain 3 protein (TIM-3) polymorphisms (-1516G/T, -574G/T, and +4259T/G) were associated with the increased risk of cancer in Chinese Han population. PMID: 27008699
  30. In cultured MART1-specific CD8 T cells stimulated with peptide-loaded artificial antigen-presenting cells, anti-TIM-3 antibody treatment promotes generation of effector T cells, with acquisition of an activated phenotype, increased cytokine production, enhanced proliferation, and a transcription program associated with T cell differentiation. Anti-TIM-3 drives CD8 T cell differentiation through activation of mTORC1. PMID: 29127145
  31. Our results show that Tim-3 is a critical negative regulator of NLRP3 inflammasome and provides a potential target for intervention of diseases with uncontrolled inflammasome activation. PMID: 28799242
  32. soluble Tim-3 might play inhibitory roles in impaired Tim-3-mediated clearance of apoptotic cells in systemic lupus erythematosus. PMID: 28754800
  33. We found a novel mechanism through which Tim-3 could suppress antitumor immunity by utilizing the suppression of CD4(+) follicular helper cells (Tfh) function and provide new insight in the regulation of Tfh cells in breast cancer patients PMID: 27156907
  34. Tim3/Gal-9 alleviates the inflammation of TAO patients via suppressing Akt/NF-kappaB signaling pathway. PMID: 28756232
  35. this study shows that severe aplastic anemia untreated patients have lower TIM-3 expression on NK cells and CD56dim NK subsets compared with normal controls, and are correlated with the severity of pancytopenia of SAA PMID: 28637584
  36. We conclude that Tim-3 is a biomarker of dysfunctional plasmacytoid dendritic cells PMID: 28264968
  37. The present study defines the minimal TIM-3 promoter region and demonstrates its interaction with c-Jun during TIM-3 transcription in CD4(+) T cells. PMID: 27243212
  38. Our findings establish intratumoral Tim-3(+)PD1(+)CD8(+) T cells as critical mediators of an aggressive phenotype in RCC. PMID: 27872087
  39. Osteosarcoma patients with higher Tim-3 had relatively lower survival. Multivariate analyses for overall survival revealed that high serum soluble Tim-3 level was an independent prognostic factor for osteosarcoma PMID: 28671022
  40. urther analyses revealed that the levels of Tim-3 on CD4+ T cells and CD8+ T cells exhibited different expression patterns in terms of localization depending on pathological category of prostate cancer and metastasis. Immunohistochemical analysis revealed that positive staining of Tim-3 in prostate cancer but little or no staining of Tim-3 was observed in benign prostate hyperplasia epithelium. PMID: 28681697
  41. this review discusses the recent findings on Tim-3, the role it plays in regulating immune responses in different cell types and the rationale for targeting Tim-3 for effective cancer immunotherapy PMID: 28258697
  42. The -1516G > T, -574G > T and +4259T > G SNPs within TIM-3 gene might play an important role as a genetic risk factor in the pathogenesis of ET. PMID: 27990849
  43. this study shows that that Tim-3 expression defines a subpopulation of PD-1+ exhausted NY-ESO-1-specific CD8+ T cell and PD-1+Tim-3+ CD8+ T cells represented the largest subset of NY-ESO-1-specific CD8+ T cells in gastric cancer patients PMID: 28110884
  44. Increased TIM3+CD8+T cells with lower perforin and granzyme B expression and higher CD95 expression in MDS patients had been observed. These findings suggested that TIM3 might be related to CD8+T cells defect. PMID: 27846431
  45. our results suggested that PD-1 and TIM-3 blockade might be necessary in developing effective immunotherapeutic strategies in malignant Schwannoma, in which TIM-3 may play a more important role. PMID: 28475007
  46. these data suggest that the high Tim-3 expression in monocytes could be utilized by tumor-promoting Gal-9 expression on CD4(+) T cells PMID: 28466780
  47. In conclusion, Tim-3 on immune cells negatively regulates cell-mediated immunity against Plasmodium infection, and blocking Tim-3 signaling enhances sterile immunity and may play a protective role during malarial parasite infections. PMID: 27638944
  48. this study shows that the transcription factor T-bet controls Tim-3-mediated inhibition of monocyte/macrophage function during chronic hepatitis C virus infection PMID: 27809352
  49. this study shows that TIM-3 expressed on myeloid leukaemia cells may facilitate functional exhaustion in T helper cells PMID: 27565576
  50. this study shows that in osteosarcoma patients, Tim3 expression did not directly mediate immune suppression, but the interaction between Tim3+ T cells and monocytes, naive CD4+ T cells, and Gal9-expressing CD4+ CD25+ Tregs could resulting in progressive suppression of Th1 responses PMID: 28103502

Show More

Hide All

Involvement in disease
May be involved in T-cell exhaustion associated with chronic viral infections such as with human immunodeficiency virus (HIV) and hepatitic C virus (HCV).
Subcellular Location
Membrane; Single-pass type I membrane protein. Cell junction. Cell membrane.
Protein Families
Immunoglobulin superfamily, TIM family
Tissue Specificity
Expressed in T-helper type 1 (Th1) lymphocytes. Expressed on regulatory T (Treg) cells after TCR stimulation. Expressed in dendritic cells and natural killer (NK) cells. Expressed in epithelial tissues. Expression is increased on CD4+ and CD8+ T-cells in
Database Links

HGNC: 18437

OMIM: 606652

KEGG: hsa:84868

STRING: 9606.ENSP00000312002

UniGene: Hs.710500

Call us
301-363-4651 (Available 9 a.m. to 5 p.m. CST from Monday to Friday)
7505 Fannin St., Ste 610, Room 322 (CUBIO Innovation Center), Houston, TX 77054, USA
Join Us with

Subscribe newsletter

Leave a message

* To protect against spam, please pass the CAPTCHA test below.
CAPTCHA verification
© 2007-2023 CUSABIO TECHNOLOGY LLC All rights reserved. 鄂ICP备15011166号-1