anti-Hepatitis A Virus Cellular Receptor 1 (HAVCR1) Antikörper

Human Hepatitis A Virus Cellular Receptor 1 (HAVCR1) Interaktionspartner

1. The urinary KIM-1 increases rapidly upon the tubular injury, and its levels are associated with the degree of tubular injury, interstitial fibrosis, and inflammation in the injured kidney.

2. In conclusion, these findings demonstrate that TIM-1 promotes Japanese encephalitis virus infection as an entry cofactor, and the polymorphism of TIM-1 is associated with Japanese encephalitis virus susceptibility to host cells.

3. neither the inflammatory biomarker calprotectin, nor the tubular biomarkers NGAL and KIM-1, provide robust prognostic information on the loss of renal function in a heterogeneous CKD population. All of them, however, are candidate prognostic biomarkers in primarily inflammatory renal diseases.

4. High KIM1 expression is associated with Clear Cell Renal Cell Carcinoma.

5. Human oligodendrocytes undergo apoptosis when exposed to Sema4A and take up H-ferritin for meeting iron requirements and that these functions are mediated via the Tim-1 receptor. H-ferritin can block Sema4A-mediated cytotoxicity. Sema4A is detectable in the CSF of multiple sclerosis patients and HIV-seropositive persons and can induce oligodendrocyte cell death.

6. Elevated plasma NT-proBNP and KIM-1 in patients with stage 5 chronic kidney disease (CKD5) undergoing maintenance hemodialysis (HD) and HF (+) (heart failure)CKD5-HD patients suggest that natriuretic peptides and KIM-1 may contribute to the pathogenesis of HF in CKD5-HD patients.

7. These findings suggest that the TIMD4-HAVCR1 variants may be the genetic risk factors for coronary heart disease and ischemic strok

8. These studies provide evidence that, in the absence of a functional alpha-dystroglycan, TIM-1 mediates the entry of Lassa virus pseudoviral particles through interactions of virions with the IgV PtdSer-binding pocket of TIM-1.

9. total flavone of Desmodium styracifolium inhibited HK-2 cell apoptosis and autophagy by regulating KIM-1 via p38/MAPK pathway.

10. 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.

11. High KIM1 expression is associated with decreased proximal tubular epithelial cell function.

12. findings show that TIM1 is not an essential cellular receptor for hepatitis A virus entry into cultured cells

13. Urinary excretion of KIM-1 correlates with blood lead levels better than other traditional renal injury biomarkers, including N-acetyl-beta-(D)-glucosaminidase, alpha1-microglobulin, and beta2-microglobulin.

14. promising results were obtained for circulating KIM-1 prediction of renal outcomes in type 1 diabetes--{REVIEW}

15. data show that in addition to the phospholipid-binding function of HAVCR1, the enhancement of HCV infection involves other determinants in the IgV domain of HAVCR1. These findings expand the repertoire of molecules that HCV uses for cell entry, adding to the already complex mechanism of HCV infection and pathogenesis.

16. Review/Meta-analysis: suggest that TIM-1-416G[C single nucleotide polymorphism is associated with the risk of asthma for the Asian ethnicity in the codominant (G/G vs. G/C) and dominant (G/G vs. G/C + C/C) genetic models.

17. Urinary NGAL is a good predictor of mortality in established pediatric acute kidney injury (AKI) of heterogeneous etiology and outperforms calprotectin and KIM-1. Urinary calprotectin and KIM-1 predict renal replacement therapy requirement in pediatric AKI.

18. A panel consisting of IGFBP1, KIM1, GCLC and GSTM1 genes could be used in combination for early screening of CKDu, whereas these genes in addition with FN1, IGFBP3 and KLK1 could be used to monitor progression of CKDu. The regulation of these genes has to be studied on larger populations to validate their efficiency for further clinical use.

19. 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.

20. Report detection of drug-induced acute kidney injury in humans by combining the sensitivity of urinary KIM-1 along with urinary miR-21, -200c, and -423.

Chimpanzee Hepatitis A Virus Cellular Receptor 1 (HAVCR1) Interaktionspartner

1. Data suggest that T-cell immunoglobulin domain and mucin domain containing protein 1 (TIM1) to be under positive natural selection in primates.

Rhesus Monkey Hepatitis A Virus Cellular Receptor 1 (HAVCR1) Interaktionspartner

1. Data suggest that T-cell immunoglobulin domain and mucin domain containing protein 1 (TIM1) to be under positive natural selection in primates.

Mouse (Murine) Hepatitis A Virus Cellular Receptor 1 (HAVCR1) Interaktionspartner

1. findings show that TIM1 is not required for hepatitis A virus (HAV) replication and pathogenesis in permissive strains of mice, although it may facilitate early stages of infection by binding phosphatidylserine on the quasi-enveloped HAV surface

2. the interaction of TIM4TIM1 was found to promote Th2cell proliferation through enhancing SIRT1 expression in mice with nasal allergic rhinitis.

3. findings provide evidence for the role of Tim-1 in the induction of a cytokine storm phenomenon and the pathogenesis of Ebola virus disease

4. Cisplatin enhances kidney injury molecule-1 (Kim-1) gene expression in kidney S3 cells.

5. By preventing ERK1/2 phosphorylation following renal injury, STAT3 phosphorylation is decreased, leading to less phosphorylated STAT3 within the nucleus, and subsequently less KIM-1 mRNA increases post injury

6. Study used a previously described highly mobile membrane mimetic membrane in combination with a conventional lipid bilayer model to generate a membrane-bound configuration of Tim1 in silico, identified two possible states for a membrane-bound form of Tim1.

7. Our data reveal a previously unknown role for Galpha12 in regulating efferocytosis and that renal tubular epithelial cells require KIM-1 to mediate this process.

8. Urinary L-FABP, NGAL, Kim-1 and albumin 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.

9. Blockade of Tim-1 changes Th1/Th2 balance and reduces circulating regulatory T cells to enhance atherosclerosis in LDL receptor knockout mice.

10. Our results suggest that KIM-1 is an endogenous protective mechanism against renal ischemia-reperfusion injury

11. data suggest that TIM-1 signaling plays a direct role in Breg maintenance and induction both under physiological conditions (in response to ACs) and in response to therapy through TIM-1 ligation

12. Deletion of the mucin 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.

13. Tim-1 is critical for maintaining self-tolerance by regulating IL-10 production in Bregs

14. blood biomarker that specifically reflects acute and chronic kidney injury

15. 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.

16. Tim-1-Fc protects cardiac grafts from chronic rejection by suppressing CD4 Th17 development and functionality.

17. KIM-1 shedding is accelerated by worsening renal cellular injury, and excess soluble KIM-1 competitively inhibits efferocytosis.

18. Endogenous Tim-1 promotes severe systemic autoimmunity and renal disease MRL-Fas(lpr) mice.

19. a major P-selectin ligand with a role in T cell trafficking during inflammatory responses and the induction of autoimmune disease

20. Sustained KIM-1 expression promotes kidney fibrosis and provides a link between acute and recurrent injury with progressive chronic kidney disease.