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Klk1b1  -  kallikrein 1-related peptidase b1

Mus musculus

 
 
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Disease relevance of Klk1b1

 

High impact information on Klk1b1

  • The stimulatory effect of TK was mimicked by bradykinin (BK) and could be reversed by application of JE049, a BK receptor type 2 antagonist [5].
  • Here, we delineated the molecular mechanism through which TK stimulates Ca(2+) reabsorption [5].
  • Interestingly, mice lacking the serine protease tissue kallikrein (TK) exhibit robust hypercalciuria comparable to the Ca(2+) leak in TRPV5 knockout mice [5].
  • Tissue kallikrein stimulates Ca(2+) reabsorption via PKC-dependent plasma membrane accumulation of TRPV5 [5].
  • Using TRPV5-expressing primary cultures of renal Ca(2+)-transporting epithelial cells, we showed that TK activates Ca(2+) reabsorption [5].
 

Chemical compound and disease context of Klk1b1

  • We tested the hypothesis that TK plays a protective role in myocardial ischemia by performing ischemia-reperfusion (IR) injury, with and without ischemic preconditioning (IPC) or ACE inhibitor (ramiprilat) pretreatment, in vivo in littermate wild-type (WT) or TK-deficient (TK-/-) mice [2].
  • Administration of aprotinin, a potent tissue kallikrein inhibitor, to STZ mice, reduced the hyperglycemia and the altered renal function of the diabetic mice to level no different from normal mice [6].
  • In the present study, a mouse fibroblast-derived packaging cell line, psi 2, which releases a replication-defective retrovirus vector bearing the herpes simplex virus type 1 (HSV)-thymidine kinase (TK) gene, was grown with rat C6 tumor cells in the presence and absence of wild type Moloney murine leukemia virus (MoMLV) [4].
 

Biological context of Klk1b1

 

Anatomical context of Klk1b1

 

Associations of Klk1b1 with chemical compounds

  • There was no difference between TK-/- and WT mice for plasma concentrations of Ca, Mg, creatinine, parathyroid hormone, or 1,25-dihydroxyvitamin D [8].
  • In addition, B2-/- mice, but not TK-/- mice, exhibited lower coronary and renal blood flows and greater corresponding vascular resistances than did WT mice, indicating a tonic physiological vasodilating effect of bradykinin in these vascular beds [9].
  • Combining PD123319 with the bradykinin B2 receptor antagonist HOE-140 had no additional effect to AT2 receptor blockade alone in TK+/+ arteries [12].
  • Ramiprilat also reduced infarct size by 29% in WT, but in TK-/- its effect was completely suppressed [2].
  • Saralasin, a nonselective angiotensin II receptor antagonist, impaired significantly flow-induced dilation in TK+/+, whereas it had no effect in TK-/- mice [12].
 

Regulatory relationships of Klk1b1

 

Other interactions of Klk1b1

 

Analytical, diagnostic and therapeutic context of Klk1b1

References

  1. Autoimmunity against a tissue kallikrein in IQI/Jic Mice: a model for Sjogren's syndrome. Takada, K., Takiguchi, M., Konno, A., Inaba, M. J. Biol. Chem. (2005) [Pubmed]
  2. Role of tissue kallikrein in the cardioprotective effects of ischemic and pharmacological preconditioning in myocardial ischemia. Griol-Charhbili, V., Messadi-Laribi, E., Bascands, J.L., Heudes, D., Meneton, P., Giudicelli, J.F., Alhenc-Gelas, F., Richer, C. FASEB J. (2005) [Pubmed]
  3. Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice. Meneton, P., Bloch-Faure, M., Hagege, A.A., Ruetten, H., Huang, W., Bergaya, S., Ceiler, D., Gehring, D., Martins, I., Salmon, G., Boulanger, C.M., Nussberger, J., Crozatier, B., Gasc, J.M., Heudes, D., Bruneval, P., Doetschman, T., Ménard, J., Alhenc-Gelas, F. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  4. An experimental model of retrovirus gene therapy for malignant brain tumors. Takamiya, Y., Short, M.P., Moolten, F.L., Fleet, C., Mineta, T., Breakefield, X.O., Martuza, R.L. J. Neurosurg. (1993) [Pubmed]
  5. Tissue kallikrein stimulates Ca(2+) reabsorption via PKC-dependent plasma membrane accumulation of TRPV5. Gkika, D., Topala, C.N., Chang, Q., Picard, N., Th??bault, S., Houillier, P., Hoenderop, J.G., Bindels, R.J. EMBO J. (2006) [Pubmed]
  6. Effects of aprotinin on the kallikrein-kinin system in type I diabetes (insulitis). Zuccollo, A., Frontera, M., Cueva, F., Navarro, M., Catanzaro, O.L. Immunopharmacology (1997) [Pubmed]
  7. Prorenin processing and restricted endoproteolysis by mouse tissue kallikrein family enzymes (mK1, mK9, mK13, and mK22). Kikkawa, Y., Yamanaka, N., Tada, J., Kanamori, N., Tsumura, K., Hosoi, K. Biochim. Biophys. Acta (1998) [Pubmed]
  8. Tissue kallikrein-deficient mice display a defect in renal tubular calcium absorption. Picard, N., Van Abel, M., Campone, C., Seiler, M., Bloch-Faure, M., Hoenderop, J.G., Loffing, J., Meneton, P., Bindels, R.J., Paillard, M., Alhenc-Gelas, F., Houillier, P. J. Am. Soc. Nephrol. (2005) [Pubmed]
  9. Cardiovascular phenotypes of kinin B2 receptor- and tissue kallikrein-deficient mice. Trabold, F., Pons, S., Hagege, A.A., Bloch-Faure, M., Alhenc-Gelas, F., Giudicelli, J.F., Richer-Giudicelli, C., Meneton, P. Hypertension (2002) [Pubmed]
  10. Role of tissue kallikrein in response to flow in mouse resistance arteries. Bergaya, S., Matrougui, K., Meneton, P., Henrion, D., Boulanger, C.M. J. Hypertens. (2004) [Pubmed]
  11. Immunohistochemical distributions of the tissue kallikrein-kinin system in ischemic and non-ischemic mouse heart. Yano, Y., Ozono, R., Nakashima, H., Oishi, Y., Kambe, M., Hosoi, K., Oshima, T. J. Cardiovasc. Pharmacol. (2003) [Pubmed]
  12. Flow-dependent dilation mediated by endogenous kinins requires angiotensin AT2 receptors. Bergaya, S., Hilgers, R.H., Meneton, P., Dong, Y., Bloch-Faure, M., Inagami, T., Alhenc-Gelas, F., Lévy, B.I., Boulanger, C.M. Circ. Res. (2004) [Pubmed]
  13. Cloning and characterization of mouse klk27, a novel tissue kallikrein expressed in testicular Leydig cells and exhibiting chymotrypsin-like specificity. Matsui, H., Moriyama, A., Takahashi, T. Eur. J. Biochem. (2000) [Pubmed]
  14. Identification of mK1, a true tissue (glandular) kallikrein of mouse submandibular gland: tissue distribution and a comparison of kinin-releasing activity with other submandibular kallikreins. Hosoi, K., Tsunasawa, S., Kurihara, K., Aoyama, H., Ueha, T., Murai, T., Sakiyama, F. J. Biochem. (1994) [Pubmed]
  15. Tissue kallikrein protects against pressure overload-induced cardiac hypertrophy through kinin B2 receptor and glycogen synthase kinase-3beta activation. Li, H.J., Yin, H., Yao, Y.Y., Shen, B., Bader, M., Chao, L., Chao, J. Cardiovasc. Res. (2007) [Pubmed]
  16. The tissue kallikrein-kinin system protects against cardiovascular and renal diseases and ischemic stroke independently of blood pressure reduction. Chao, J., Bledsoe, G., Yin, H., Chao, L. Biol. Chem. (2006) [Pubmed]
  17. Plasminogen-independent initiation of the pro-urokinase activation cascade in vivo. Activation of pro-urokinase by glandular kallikrein (mGK-6) in plasminogen-deficient mice. List, K., Jensen, O.N., Bugge, T.H., Lund, L.R., Ploug, M., Danø, K., Behrendt, N. Biochemistry (2000) [Pubmed]
  18. Developmental and androgenic regulation of the immunocytochemical distribution of mK1, a true tissue kallikrein, in the granular convoluted tubule of the mouse submandibular gland. Kurabuchi, S., Hosoi, K., Gresik, E.W. J. Histochem. Cytochem. (2002) [Pubmed]
 
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