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Human KLKB1 ELISA Kit for Sandwich ELISA - ABIN578408
Lee, Joo, Lim, Park, Lee, Park, Seok, Lee, Kang: Proteomic analysis of serum from patients with major depressive disorder to compare their depressive and remission statuses. in Psychiatry investigation 2015
Microenvironmental acidity determines qualitatively and quantitatively the release of extracellular vesicles by malignant prostate tumors. This leads to the spill-over of nanovesicles into the peripheral blood of prostate cancer patients, where the levels of tumor biomarkers expressed by exosomes, such as PSA-exosomes, may represent a novel, non-invasive diagnostic tool.
these data indicate that KLKB1 induces inflammatory reactions in human dental tissues via protease-activated receptor 1 (show F2R ELISA Kits)
Promoter methylation of MCAM, ERalpha and ERbeta have a potential to be utilized as biomarker for the early detection of prostate cancer (PC) as their sensitivity and specificity seem to be better than serum PSA.
Data suggest no influence of chronic periodontitis treatment on PSA levels in asymptomatic men.
Circulating total PSA levels were strongly associated to leukocyte telomere length in a national sample of men without prostate cancer.
I might also point out that whether a particular surgical procedure did more good than harm at that time was highly dependent on whether it was conducted with good sterile procedure. PSA screening is a contemporary example of this historical lesson
Data show that forkhead box M1 protein (FOXM1) directly binds to the FHK binding motifs in the prostate specific antigen (PSA) promoter/enhancer regions.
Study suggests that the prognostic value of PSA declines in heavily treated patients receiving enzalutamide
novel urinary gene expression signature that may be the least invasive of available options by not requiring a digital rectal examination or phlebotomy as a reflex test in men for whom PSA testing raises the suspicion of prostate cancer
For PSA screening to be cost-effective, it needs to be used conservatively and ideally in combination with a conservative management approach for low-risk disease
Plasma kallikrein mediates brain hemorrhage and edema caused by tissue plasminogen activator (show PLAT ELISA Kits) therapy in mice after stroke.
we found that post-ejaculated semen from fertile wild-type males was solidified and the sperm were entrapped in Wnt7aCre/+;Esr1f/f uteri, compared to the watery semen (liquefied) found in Esr1f/f controls.Kallikrein-related peptidases 3 (KLK3 (show PSA ELISA Kits)) and other kallikrein (show KLK1 ELISA Kits)-related peptidases from male prostate glands are responsible for semen liquefaction by cleaving gel-forming proteins
Klkb1(-/-) mice have a novel mechanism for thrombosis protection in addition to reduced contact activation. This pathway arises when bradykinin delivery to vasculature is compromised and mediated by increased receptor Mas (show MAS1 ELISA Kits), prostacyclin, Sirt1 (show SIRT1 ELISA Kits), and KLF4 (show KLF4 ELISA Kits)
Plasma kallikrein deletion prevents occlusive thrombus formation in mice with a minimal role in provoked bleeding.
PKK (show RIPK4 ELISA Kits) or fXII (show F12 ELISA Kits) deficiency reduced thrombus formation in both arterial and venous thrombosis models, without an apparent effect on hemostasis.
Data suggest that LGG secreting PSA (show NPEPPS ELISA Kits) may activate antigen specific immune responses when instilled intravesically and IL15 (show IL15 ELISA Kits) could enhance this response.
the prekallikrein gene (Klkb1) is expressed highly in the mammary gland during stromal remodeling periods including puberty and postlactational involution.
Plasma prekallikrein is a glycoprotein that participates in the surface-dependent activation of blood coagulation, fibrinolysis, kinin generation and inflammation. It is synthesized in the liver and secreted into the blood as a single polypeptide chain. Plasma prekallikrein is converted to plasma kallikrein by factor XIIa by the cleavage of an internal Arg-Ile bond. Plasma kallikrein therefore is composed of a heavy chain and a light chain held together by a disulphide bond. The heavy chain originates from the amino-terminal end of the zymogen and contains 4 tandem repeats of 90 or 91 amino acids. Each repeat harbors a novel structure called the apple domain. The heavy chain is required for the surface-dependent pro-coagulant activity of plasma kallikrein. The light chain contains the active site or catalytic domain of the enzyme and is homologous to the trypsin family of serine proteases. Plasma prekallikrein deficiency causes a prolonged activated partial thromboplastin time in patients.
, prostate specific antigen
, prostate-specific antigen
, Fletcher factor
, plasma kallikrein
, plasma kallikrein heavy chain
, plasma kallikrein light chain
, plasma prekallikrein
, antigen, prostate specific
, fletcher factor
, kallikrein 3, plasma
, kallikrein B, plasma (Fletcher factor) 1
, Plasma kallikrein
, plasma kallikrein-like
, SH2 and PH domain-containing adapter protein APS
, SH2B adapter protein 2
, adapter protein with pleckstrin homology and Src homology 2 domains
, adaptor protein with pleckstrin homology and src homology 2 domains