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The protein encoded by HAVCR1 is a membrane receptor for both human hepatitis A virus (HHAV) and TIMD4. Additionally we are shipping HAVCR1 Kits (81) and HAVCR1 Proteins (36) and many more products for this protein.
Showing 10 out of 171 products:
Human Monoclonal HAVCR1 Primary Antibody for CyTOF, FACS - ABIN4899579
Ivie, Fennessey, Sheng, Rubin, McClain: Gene-trap mutagenesis identifies mammalian genes contributing to intoxication by Clostridium perfringens ε-toxin. in PLoS ONE 2011
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Human Monoclonal HAVCR1 Primary Antibody for CyTOF, FACS - ABIN4899580
Kuroda, Fujikura, Noyori, Kajihara, Maruyama, Miyamoto, Yoshida, Takada: A polymorphism of the TIM-1 IgV domain: implications for the susceptibility to filovirus infection. in Biochemical and biophysical research communications 2014
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Mouse (Murine) Polyclonal HAVCR1 Primary Antibody for ICC, IHC - ABIN1077715
Schindler, Bondeva, Schindler, Claus, Franke, Wolf: Preconditioned suppression of prolyl-hydroxylases attenuates renal injury but increases mortality in septic murine models. in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2016
Data suggest that T-cell immunoglobulin domain and mucin (show SLC13A2 Antibodies) domain containing protein 1 (TIM1 (show TIMELESS Antibodies)) to be under positive natural selection in primates.
Our data reveal a previously unknown role for Galpha12 (show GNA12 Antibodies) in regulating efferocytosis and that renal tubular epithelial cells require KIM-1 to mediate this process.
Urinary L-FABP (show FABP1 Antibodies), NGAL (show LCN2 Antibodies), Kim-1 and albumin (show ALB Antibodies) levels increased during the acute phase of kidney injury and were significantly correlated with the degree of tubulointerstitial fibrosis during the chronic phase. These markers could detect higher risk of progression to CKD.
Blockade of Tim-1 changes Th1 (show HAND1 Antibodies)/Th2 balance and reduces circulating regulatory T cells to enhance atherosclerosis in LDL receptor (show LDLR Antibodies) knockout mice.
Our results suggest that KIM-1 is an endogenous protective mechanism against renal ischemia-reperfusion injury
data suggest that TIM-1 signaling plays a direct role in Breg maintenance and induction both under physiological conditions (in response to ACs (show Acsl1 Antibodies)) and in response to therapy through TIM-1 ligation
Deletion of the mucin (show SLC13A2 Antibodies) domain impaired KIM-1-mediated phagocytic function, resulting in increased proinflammatory cytokine production, decreased antiinflammatory growth factor secretion by proximal epithelial cells, and an increase in tissue macrophages.
Tim-1 is critical for maintaining self-tolerance by regulating IL-10 (show IL10 Antibodies) production in Bregs
Tim-1 expression was lower in a herpes simplex virus-induced Behcet's disease (BD) mouse model compared to that in asymptomatic BD normal (BDN) mice.
Tim-1-Fc protects cardiac grafts from chronic rejection by suppressing CD4 (show CD4 Antibodies) Th17 development and functionality.
KIM-1 shedding is accelerated by worsening renal cellular injury, and excess soluble KIM-1 competitively inhibits efferocytosis.
Urine KIM-1 level in acute kidney injury patients was significantly higher than that in the healthy controls.
PCNSL is characterized by frequent Tim-1 (show ARHGEF5 Antibodies) expression, and its soluble form in CSF (show CSF2 Antibodies) may become a useful biomarker for PCNSL.
TIM-1 (show ARHGEF5 Antibodies) is a unique marker for the identification of a human IL-10 (show IL10 Antibodies)(+) Breg subpopulation which is partially superimposed with transitional B cells
in the current meta-analysis, based on ten prospective studies involving 29366 participants, we evaluated the role of urinary tubular injury markers (NGAL (show LCN2 Antibodies), KIM-1 and NAG (show NAGLU Antibodies)) in predicting clinical outcomes including CKD stage 3, end stage renal disease and mortality.
Urinary KIM-1 levels in the acute kidney injury (AKI) preterm infant group were not significantly higher than in no-AKI group on day of life 1, 3 and 7.
We conclude that KIM-1 might serve as a sensitive biomarker to screen children for kidney damage induced by environmental toxic agents, such as chromium and arsenic
These results suggest that a 6-amino acid deletion polymorphism in the mucin (show SLC13A2 Antibodies) domain of TIM-1 (show ARHGEF5 Antibodies) protects from HIV-1 infection with a recessive effect.
The present study shows that serum and urine levels of NGAL (show LCN2 Antibodies) and KIM-1 are higher in patients with acute kidney injury than in those without acute kidney injury, and that serum NGAL (show LCN2 Antibodies) and the presence of chronic kidney disease are significant predictors of acute kidney injury in scrub typhus.
KIM-1 increases albumin (show ALB Antibodies) endocytosis in renal tubule epithelial cells.
preliminary data indicates that KIM-1 expression may be associated with stage in Wilms Tumor
The protein encoded by this gene is a membrane receptor for both human hepatitis A virus (HHAV) and TIMD4. The encoded protein may be involved in the moderation of asthma and allergic diseases. The reference genome represents an allele that retains a MTTVP amino acid segment that confers protection against atopy in HHAV seropositive individuals. Three transcript variants encoding the same protein have been found for this gene.
hepatitis A virus cellular receptor 1
, T-cell immunoglobulin and mucin domain containing 1
, hepatitis A virus cellular receptor 1 homolog
, kidney injury molecule 1
, t cell immunoglobulin and mucin domain-containing protein 1
, t cell membrane protein 1
, T cell immunoglobin domain and mucin domain protein 1
, T-cell membrane protein 1
, rho guanine nucleotide exchange factor 5