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

Human Hepatitis A Virus Cellular Receptor 1 (HAVCR1) Interaktionspartner

1. We demonstrated that BDNF is essential for glomerular development, morphology and function and the expression of BDNF and KIM-1 is highly correlated in urine cells of chronic kidney disease patients.

2. Plasma KIM-1 concentrations could predict RCC incidence up to 5 years prior to diagnosis and were associated with poorer survival.

3. expression of Tctex-1 T94E did not influence KIM-1-mediated efferocytosis

4. KIM-1 is a specific and stable marker of antemortem tubular injury in kidneys of adults and fetuses despite postmortem autolysis.

5. uKIM-1 increased significantly after a very short period of exercise. It is not clear if the increase in KIM-1 is caused by post-exercise albuminuria

6. KIM-1 is the most sensitive biomarker for early detection of acute kidney injury in patients receiving platinum based drugs.

7. Serum kidney injury molecule 1 and beta2-microglobulin perform as well as larger biomarker panels for prediction of rapid decline in renal function in type 2 diabetes.

8. The 157insMTTTVP variant of HAVCR1 gene was not associated with more severe outcome of hepatitis A virus infection in an Indian population.

9. The urinary KIM-1 level corresponds with the severity of renal histological damage and can be a potential reliable predictor of adverse renal outcomes in acute tubular injury (ATI) patients. Moreover, combining urinary and plasma KIM-1 levels can increase the sensitivity and specificity of the diagnosis of severe ATI.

10. HAVCR1 upregulation might serve as a valuable prognostic marker in terms of OS and RFS in GC patients

11. We used the CRISPR/Cas9 system to knock-in reporter transgenes at the kidney injury molecule-1 (KIM-1) locus and isolated proximal tubule cell (HK-2) clones. PCR verified targeted knock-in of the luciferase and eGFP reporter at the KIM-1 locus. HK-2-KIM-1 reporter cells responded to various stimuli including hypoxia, cisplatin, and high glucose, indicative of upregulation of KIM-1 expression.

12. 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.

13. 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.

14. 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.

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

16. 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.

17. 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.

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

19. 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.

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

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. These studies provide evidence that at late times during Ebola virus glycoprotein/recombinant vesiculovirus infection, TIM-1 increased virus load and associated mortality, consistent with an important role of this receptor in virus entry.

2. Our findings suggest a role for UMOD-dependent inhibition of KIM-1 expression and its apoptotic cell scavenging responses during chronic obstruction-associated tubular injury

3. 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

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

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

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

7. 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

8. 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.

9. 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.

10. 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.

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

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

13. 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

14. 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.

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

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

17. 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.

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

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

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