Disease relevance of ESFENVALERATE

• Two independent experimental strategies are employed: the ability of 12 monoclonal antibodies to recognize L cell transfectants bearing chimeric and mutant A alpha chains is assessed, and the amino acid sequences of A alpha chains expressed by immunoselected B lymphoma mutants are deduced [1].
• The crystallographic structure of Neisseria gonorrhoeae pilin, which assembles into the multifunctional pilus adhesion and virulence factor, reveals an alpha-beta roll fold with a striking 85 A alpha-helical spine and an O-linked disaccharide [2].
• Juveniles and young adult A alpha-/- mice are predisposed to spontaneous fatal abdominal hemorrhage, but long-term survival is variable and highly dependent on genetic background [3].
• In this report we show that substituting alanines at all but five amino acids in the myelin basic protein (MBP) peptide Ac1-11 does not alter its ability to bind A alpha uA beta u (MHC class II molecules), to stimulate specific T cells and, surprisingly, to induce experimental autoimmune encephalomyelitis (EAE) in (PL/J x SJL/J)F1 mice [4].
• Two families with hereditary renal amyloidosis were found to have a novel mutation in the fibrinogen A alpha chain gene [5].

Psychiatry related information on ESFENVALERATE

• The role of A alpha chain is also implied by the permissiveness of E kappa alpha Aq beta but not Aq alpha Aq beta molecules in the deletion of V beta 6+ T cells [6].
• Hyperphosphorylated tau, the major component of the paired helical filaments of Alzheimer's disease, was found to accumulate in the brains of mice in which the calcineurin A alpha gene was disrupted [calcineurin A alpha knockout (CNA alpha -/-)] [7].

High impact information on ESFENVALERATE

• Mixed isotype (E alpha A beta and A alpha E beta) dimers are not found on Ia+ hematopoietic cells, although some pairs (e.g., E alpha A beta d) reach the membrane of transfected cells expressing only the two relevant class II genes [8].
• We have now isolated and sequenced A alpha cDNA clones from five other mouse haplotypes: d, b, f, u, and q [9].
• Regions of allelic hypervariability in the murine A alpha immune response gene [9].
• The structure of one of these class II major histocompatibility complex molecules, A alpha, was recently deduced from sequence analysis of a cDNA clone produced from k haplotype mice [9].
• The genes encoding the alpha- and beta-chains of the class II heterodimers, A alpha A beta and E alpha E beta, have recently been characterized at the molecular level, and certain cloned genes were shown to be functionally expressed after introduction into cells by DNA-mediated gene transfer [10].

Chemical compound and disease context of ESFENVALERATE

• Chloramphenicol acetyltransferase gene expression was cis-activated by a region of the Ia A alpha k gene in a B lymphoma line, but not in a myeloma line [11].
• Cyanase, an oligomeric enzyme of Escherichia coli that catalyzes the decomposition of cyanate to ammonia and bicarbonate, crystallizes in the space group P1 with unit cell parameters a = 85.96 A, b = 83.17 A, c = 83.28 A, alpha = 110.29 degrees, beta = 118.29 degrees and gamma = 72.40 degrees [12].
• Active site mapping of the serine proteases human leukocyte elastase, cathepsin G, porcine pancreatic elastase, rat mast cell proteases I and II. Bovine chymotrypsin A alpha, and Staphylococcus aureus protease V-8 using tripeptide thiobenzyl ester substrates [13].
• Cyclosporin A/alpha interferon-induced autologous graft-versus-host disease following peripheral blood stem cell transplant for chronic myeloid leukaemia: a clinico-pathological study [14].
• Prominent neurologic signs and moderate retardation of body weight were observed in the groups given 1500 ppm fenvalerate and 500 ppm esfenvalerate, although no adverse effects on survival were evident [15].

Biological context of ESFENVALERATE

• These data on the effects of allelic variation on Ia levels provide a possible explanation for the strong linkage disequilibrium of A alpha and A beta genes and may account for the current molecular organization of the I region of the MHC [16].
• The activation of T helper lymphocytes involves the recognition of class II major histocompatibility complex antigens, which are dimeric glycoproteins (of subunit composition A alpha A beta or E alpha E beta) expressed on the surfaces of macrophages and B lymphocytes [17].
• All of the component chains of fibrinogen (A alpha, B beta, and gamma) are immunologically undetectable in the circulation of both neonatal and adult A alpha-/- mice, and blood samples fail to either clot or support platelet aggregation in vitro [3].
• The combination of dissimilar alleles of the A alpha and A beta gene complexes, whose proteins contain homeo domain motifs, determines sexual development in the mushroom Coprinus cinereus [18].
• To explore the role of the key coagulation factor, fibrinogen, in development, hemostasis, wound repair, and disease pathogenesis, we disrupted the fibrinogen A alpha chain gene in mice [3].

Anatomical context of ESFENVALERATE

• Overt bleeding events develop shortly after birth in approximately 30% of A alpha-/- mice, most frequently in the peritoneal cavity, skin, and soft tissues around joints [3].
• The periodic rupture of ovarian follicles in breeding-age A alpha-/- females does not appear to significantly diminish life expectancy relative to males; however, pregnancy uniformly results in fatal uterine bleeding around the tenth day of gestation [3].
• T cell responses in calcineurin A alpha-deficient mice [19].
• In this report, we have demonstrated that IFN-gamma and TNF-alpha increase expression of both the I-A and I-E region gene products on the surface of the myelomonocytic cell line WEHI-3, and that they mediate this increase via an increase in A alpha transcription [20].
• By screening for inhibition of antigen presentation to NOD T cell hybridoma, we have selected a synthetic peptide, yTYTVHAAHAYTYt (small letters denote D amino acids), that efficiently blocks antigen presentation by the NOD class II MHC molecule A alpha g7A beta g7 (Ag7) in vitro [21].

Associations of ESFENVALERATE with other chemical compounds

• Autoradiography of the display of EC-bound 125I on polyacrylamide gel showed the constitutive B beta- and gamma-chains of the fg molecule, with a partial loss of the A alpha-chain [22].
• We have found that chymotrypsin A alpha is also inhibited by heparin cofactor II with a second-order rate constant value of 1.8 X 10(6) M-1 X min-1 at pH 8.0 and 25 degrees C. However, there was no measurable effect of heparin or dermatan sulfate on the rate of chymotrypsin inhibition [23].
• Thus, CD11c/CD18 on tumor necrosis factor-stimulated neutrophils functions as a fibrinogen receptor that recognizes the sequence Gly-Pro-Arg in the N-terminal domain of the A alpha chain of fibrinogen [24].
• Amino acid sequence analysis of the abnormal peptide indicated that A alpha proline-18, the second residue from the NH2-terminus of the fibrin alpha-chain, was replaced by leucine [25].
• The basal level of lung cell gamma-FBG gene transcription was not accompanied by appreciable levels of A alpha and B beta chain gene transcription; however, nuclear run-on analysis suggested that the increase in lung cell FBG mRNAs in response to DEX +/- IL-6 was due to new transcription [26].

Gene context of ESFENVALERATE

• Three of the four chains, A alpha, A beta and E beta, are controlled by loci in the I-A subregion, whereas the locus controlling the E alpha chain is located in the I-E subregion of the H-2 complex [27].
• Mutants mice carrying targeted inactivations of both retinoic acid receptor (RAR) alpha and RAR gamma (A alpha/A gamma mutants) were analyzed at different embryonic stages, in order to establish the timing of appearance of defects that we previously observed during the fetal period [28].
• The hindbrain of E8.5 A alpha/A gamma embryos shows a posterior expansion of rhombomere 3 and 4 (R3 and R4) markers, but fails to express kreisler, a normal marker of R5 and R6 [28].
• At the nucleotide level Drosophila calcineurin A cDNA is 67 and 65% identical to human calcineurin A alpha and beta cDNAs, respectively [29].
• CD4(+) alpha beta T cells from either normal C57BL/6 (B6) or MHC-II-deficient (A alpha(-/-) or A beta(-/-)) B6 donor mice engrafted into congenic immunodeficient RAG1(-/-) B6 hosts induced an aggressive inflammatory bowel disease (IBD) [30].

Analytical, diagnostic and therapeutic context of ESFENVALERATE

• Functional sites on Ia molecules: a molecular dissection of A alpha immunogenicity [1].
• Northern blot analyses indicated that one I-A-, I-E+ tumor strongly expressed A alpha, E alpha, and E beta mRNAs but possessed only a weak expression of A beta mRNA [31].
• By immunoprecipitation and two-dimensional analysis of Ia molecules from F1 spleen cells, we could independently map the reactivities of the mAb as being determined by the A alpha or A beta chain [32].
• In addition to FPB release, SDS-PAGE analysis of the time course of urokinase-mediated fibrinogenolysis indicates progressive proteolysis of both the A alpha- and B beta-chains of fibrinogen that occurs after FPB release is completed [33].
• By separating the products of HNE digestion of fibrinogen using high performance liquid chromatography, identifying the immunoreactive fractions and subjecting them to amino acid analysis, the fragment was identified as A alpha 1-21, indicating an HNE cleavage site at the Val(A alpha 21)-Glu(A alpha 22) bond [34].

References