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Gene Review

CPA6  -  carboxypeptidase A6

Homo sapiens

Synonyms: CPAH, Carboxypeptidase A6, ETL5, FEB11
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Disease relevance of CPA6


Psychiatry related information on CPA6


High impact information on CPA6

  • To examine whether T cells can produce met-enkephalin precursor peptides, T cell conditioned media were treated with trypsin and carboxypeptidase-B, which is known to release met-enkephalin from the propeptide [7].
  • We have optimized conditions for measurement of immunoreactive Met-enkephalin in plasma and for generation by trypsin and carboxypeptidase B of much greater amounts of total peptidase-derivable Met-enkephalin in plasma of rats, dogs, and humans [8].
  • In contrast, clot lysis by t-PA was unaffected by plasmin pretreatment and little affected by carboxypeptidase B treatment of the fibrin substrate [9].
  • Promotion by plasmin was nullified by a subsequent treatment of the clot with carboxypeptidase B, indicating that the plasmin effect was related to the exposure of carboxy terminal lysine residues on fibrin [9].
  • The immunoreactive kinin in nasal washes was stable to boiling and not precipitated by ethanol, but completely destroyed by carboxypeptidase B. It was evenly distributed between the sol and gel phases of nasal washes [10].

Chemical compound and disease context of CPA6


Biological context of CPA6

  • The CP on chromosome 8 is predicted to have a CPA-like specificity for C-terminal hydrophobic residues and was named CPA6 [16].
  • RESULTS: A carboxypeptidase gene (CPAH) was directly interrupted between the first and second exons in a patient with DURS who carried a de novo reciprocal balanced translocation t(6;8)(q26;q13) involving the DURS1 region on chromosome arm 8q13 [17].
  • The blood glucose concentration was not significantly altered, and there was no change in the filtered load of glucose; glomerular filtration rate (CIN) and renal plasma flow (CPAH) were unchanged [18].
  • Thrombin activatable fibrinolysis inhibitor (TAFI) is a carboxypeptidase B-like proenzyme that after activation down-regulates fibrinolysis [19].
  • Equilibrium binding analysis and [Lys]Pg activation kinetics with wild-type SK, carboxypeptidase B-treated SK, and a COOH-terminal Lys(414) deletion mutant (SKDeltaK414) demonstrated a critical role for Lys(414) in the enhancement of [Lys]Pg and [Lys]Pm binding and conformational [Lys]Pg activation [20].

Anatomical context of CPA6


Associations of CPA6 with chemical compounds

  • Release of carboxyl-terminal arginine residue by carboxypeptidase B, converting C3a into des-Arg77-C3a, did not alter the inhibitory effect displayed by this fragment [26].
  • When tested with hippurylarginine, hippurylargininic acid, benzoylalanyllysine, or bradykinin, the Mr 48,000 subunit was as active as the intact enzyme and was easily distinguished from human pancreatic carboxypeptidase B (EC [27].
  • The variant COOH terminus ends with the dibasic sequence Arg-Lys that is apparently removed through stepwise cleavage by serum carboxypeptidase B to yield several forms of circulating albumin [28].
  • The resulting benzyloxycarbonyl derivatives of isoglutaminylarginine methyl ester and isoasparaginylarginine methyl ester were treated with trypsin for removal of the ester groups and then with porcine pancreatic carboxypeptidase B for liberation of arginine and the original benzyloxycarbonyl derivatives of isoglutamine and isoasparagine [29].
  • The immunochemical detection of these FPB-related peptides should provide useful information concerning the action of proteolytic enzymes, such as plasmin on the NH2-terminal segment of the B beta-chain of fibrinogen, and of carboxypeptidase-B on free FPB, in human plasma [30].

Physical interactions of CPA6


Enzymatic interactions of CPA6


Regulatory relationships of CPA6


Other interactions of CPA6


Analytical, diagnostic and therapeutic context of CPA6

  • Insulin infusion did not affect Cin, increased CPAH (p < 0.05) and, consequently, lowered the filtration fraction (p < 0.01) in both groups [40].
  • New bands appearing at pI 6.65 and 6.75 after treatment of sMi-CK with carboxypeptidase B were found to be delysined forms. sMi-CK reacted with anti-sMi-CK antibodies, and the immune complexes were focused at pI 5 [41].
  • Donor CPAH prior to donation was significantly correlated with the renal allograft function of the recipients but not with the recipient ranked MAP at follow-up [42].
  • Studies were performed with IPS (mean airway pressure 12-15 cm H2O), continuous positive airway pressure (CPAP 6 cm H2O), and with oxygen (2 l/min via a mask) in random order on three separate days [43].
  • We measured ambulatory 24-hour blood pressure (SpaceLab system), echocardiography (ASE criteria, Acuson 128 XP 10), CIn and CPAH, urinary Na excretion, PRA and insulin concentration [44].


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  20. Binding of the COOH-terminal Lysine Residue of Streptokinase to Plasmin(ogen) Kringles Enhances Formation of the Streptokinase{middle dot}Plasmin(ogen) Catalytic Complexes. Panizzi, P., Boxrud, P.D., Verhamme, I.M., Bock, P.E. J. Biol. Chem. (2006) [Pubmed]
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  26. Inhibition of in vitro natural killer activity by the third component of complement: role for the C3a fragment. Charriaut, C., Senik, A., Kolb, J.P., Barel, M., Frade, R. Proc. Natl. Acad. Sci. U.S.A. (1982) [Pubmed]
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