Aperçu des produits pour anti-Kallikrein 1 (KLK1) Anticorps

Human Kallikrein 1 (KLK1) interaction partners

1. Letter: KLK1 (rs5516) was associated with thoracic aortic dissection.

2. Our findings suggest that the A2233C polymorphism of KLK1 may be a marker of evaluation of hypertensive subjects' responses to angiotensin I converting enzyme inhibitors benazepril.

3. Recognition of anti-tumor necrosis factor-alpha (TNF-alpha) or Kallikrein Inhibitor may lead to therapeutics to enhance existing treatments for patients who do not respond to anti-vascular endothelial growth factor (VEGF) therapies.

4. increasing the serum levels of AngII increased the risk of acute myocardial infarction (AMI); the risk of AMI increased when the serum levels of AngII and KLK1 simultaneously increased; individuals with the combined genotypes of ACE DD and KLK1 GG showed increased risk of AMI compared with those with the combined genotypes of ACE II and KLK1 AA

5. The rs5516 G allele of KLK1 was significantly associated with aortic aneurysm

6. KLK1 rs5516 SNP is not related to the incidence of Alzheimer's disease in a Hunan Han Chinese population.

7. TK promoted cell survival and beta-catenin degradation in serum-starved SH-SY5Y cells via increasing autophagy.

8. Our findings suggest that higher levels of TK in plasma are associated with the presence of CAD and are a predictor of mild coronary arteriosclerosis.

9. The kallikrein system in retinal damage/protection

10. Preclinical characterization of recombinant human tissue kallikrein-1 as a novel treatment for type 2 diabetes mellitus.

11. Up-regulation of KLK1 in tubular epithelial cells may mediate pro-inflammatory pathway and PAR activation during diabetic nephropathy.

12. These data do not support a role for the Tissue kallikrein-kinin system, protective or deleterious, in the development of insulin resistance and diabetes.

13. Tissue kallikrein facilitated the activation of EGFR, ERK1/2 and p38 cascade. Not p38 but ERK1/2 phosphorylation was severely compromised in cells depleted of EGFR. Impairment of signaling of ERK1/2 seemed not to be restricted to EGFR phosphorylation.

14. allele H is a common polymorphism in Japanese and may contribute to decreased reabsorptions of calcium and sodium in the kidney

15. Data suggest factor XII binding/autoactivation are increased on surface of hantavirus-infected vascular endothelium; thus, activation of kallikrein-kinin system during hantavirus infection could have profound implications on capillary permeability.

16. Tissue kallikrein-modified mesenchymal stem cells provide enhanced protection against ischemic cardiac injury after myocardial infarction.

17. KLK1 promoter polymorphisms are associated with development of AKI and adverse outcomes. Further studies are needed to validate these findings.

18. Polymorphism of the KLK1 A1789G gene is associated with coronary artery stenosis.

19. Unexpectedly, elevated KLK1 expression and excretion is found in patients with established or incipient acute kidney injury.

20. Suggest that a genetic polymorphism in KLK1 may contribute to the risk of developing later stage abdominal aortic aneurysm.

Mouse (Murine) Kallikrein 1 (KLK1) interaction partners

1. Polypeptides identified based on immunorecognition by autoantibodies in sera from IQI/Jic mice affected with autoimmune disease (>12 weeks of age) were tissue kallikrein (Klk)-1 and -13 and were cross-reactive to the autoantibodies.

2. Protective effects of Tissue kallikrein gene transfer on ischemic diseases.

3. TK, like several other proteases, can activate ENaC in the kidney and the colon.

4. Tissue kallikrein and kinins do not influence the trophicity of kidneys, the synthesis and secretion of renin, blood pressure increase, and cardiac remodeling due to renin angiotensin system activation.

5. tissue kallikrein knockout mice had a significant two-fold increase in albuminuria

6. The study suggests that kallikrein plays an antihypertensive role in hyperaldosteronism.

7. These data do not support a role for the TK-kinin system, protective or deleterious, in the development of insulin resistance and diabetes.

8. Lower excretion of active renin and prorenin in TK(-/-) compared to TK(+/+) suggest coordinated regulation of the two proteins in their participation to collecting duct function.

9. Plasma kallikrein-deficient mice challenged with transient middle cerebral artery occlusion developed significantly smaller brain infarctions.

10. Local expression of kallikreins within the kidney has the capacity to dampen lupus nephritis, possibly by modulating inflammation and oxidative stress.

11. The data of this study presented support the conclusion that Klk6 is an important participant in the immunopathogenic events that drive TMEV-IDD at acute through early chronic time points.

12. Tissue kallikrein is essential for invasive capacity of circulating proangiogenic cells.

13. kallikrein 6 is expressed in the nonmalignant and malignant prostate, with cancer tissues demonstrating slightly lower expression

14. Kallikrein 6 participates in enzymatic cascades mediating CNS inflammatory disease.

15. Tissue-specific expression patterns and differential regulation in CNS disease indicates that each K6 5'-transcript is probably regulated by unique promoter elements and may serve as a molecular target to treat inflammatory demyelinating disease.

16. Data suggest that tissue kallikrein 1 may be implicated in the growth of uterine endometrial tissues during the proliferative phase.

17. These results suggest that LPS activates the kallikrein-kinin system in the choroid plexus via autocrine induction of IL-1beta and TNF-alpha.

18. role of KLK1 in arterial function; role of KLK1 in the control of ionic transport in the renal tubule; cardio- and nephro-protective effects of KLK1 and kinins in acute cardiac ischemia, post-ischemic heart failure, and diabetes [review]

19. KLK6, but not KLK1 is an activator of CNS protease-activated receptors

20. Gene-transfer of wild-type Ad.hKLK1 (kallikrein 1) was able to rescue impaired muscle neovascularization in hindlimb ischemia in knockout mice