Disease relevance of IGKV2-24

• The toxicity to neutrophils and lymphocytes was demonstrated by decreased lactate production (LP) after incubation with A23 of Ficoll-Hypaque fractions greatly enriched in each respective cell type [1].
• All A23 transgenic animals spontaneously developed severe autoimmune gastritis, and evidence of disease was detected as early as day 10 of life [2].
• PATIENT: A 23-year-old woman with monthly recurrent meningitis episodes, mostly in the perimenstrual period, since August 1999 [3].
• CASE: A 23-year-old woman, para 2-0-0-2, developed hepatitis A at 20 weeks' gestation [4].
• The 323/A23 monoclonal antibody (MAb) is expressed with increasing breast atypia, whilst Ca1 has been suggested as a marker of cancer risk in benign breast disease [5].

Psychiatry related information on IGKV2-24

• A22, A23, and A39 provide major afferents to other frontal systems and have previously been implicated in very early clinical Alzheimer's disease [6].
• The transition to clinical dementia was associated with the presence of tauopathy in A9/10, A22, A23, and A39 [6].

High impact information on IGKV2-24

• In this report we identify HCV-specific CTL responses restricted by the HLA class I molecules A2, A3, A11, A23, B7, B8, and B53 [7].
• However, ionophore A23 187 released similar levels of histamine from the 2 MC types [8].
• We now show that molecular modeling of tyrphostin A23 into the tyrosine-binding pocket in mu2 provides a structural explanation for A23 being able to inhibit the interaction between YXXPhi motifs and mu2 [9].
• These data are consistent with A23 inhibition of the YXXPhi motif/mu2 interaction in intact cells and with the possibility that different tyrphostins may be used to inhibit specific membrane trafficking events in eukaryotic cells [9].
• Pretreatment with VO(4)(-3) antagonized genistein-induced augmentation and A23- or A25-induced suppression of I(Cl.vol) [10].

Chemical compound and disease context of IGKV2-24

• Toxicity to basophils was considered to be manifested by the increasing inability of 2-deoxyglucose (2DG) to inhibit histamine release (HR) at increasing concentrations of A23 [1].

Biological context of IGKV2-24

• Immunogenetic investigation demonstrated that HLA-A11 and A23 were significantly overrepresented in the whole group of cryptorchids in comparison with the controls (P = 0.004 and P = 0.0123, respectively) [11].
• Due to the complete penetrance of spontaneous disease, identity of the auto-antigen, susceptibility to immunoregulation, and close relation to autoimmune gastritis in man, A23 transgenic mice represent a unique CD4(+) T cell-mediated disease model for understanding the multiple factors regulating organ-specific autoimmunity [2].
• All individuals utilized either the Vkappa A23 L chain, the Vkappa L6 L chain, or both chains in forming the 23F-specific combining site [12].
• We have constructed a set of hybrid cell lines by irradiation of GM 64063 (human chromosome 9q only on hamster background) and fusion to hamster A23 Tk-, 109 independent lines were tested by PCR with 24 markers from chromosome 9q [13].
• A radiation hybrid panel has been constructed for chromosome 9 using the somatic cell hybrid GM10611 as the donor cell line fused to the hamster cell line A23 [14].

Anatomical context of IGKV2-24

• In 18 patients with OSA the release of superoxide from polymorphonuclear neutrophils was determined after stimulation with the bacterial tripeptide formylmethionylleucylphenylalanine (fMLP) and the calcium ionophore A23 [15].
• Red cells present in dextran-sedimented leukocytes were increasingly susceptible to lysis during washing subsequent to exposure to increasing concentrations of A23 [1].
• The T cell receptor alpha and beta genes from this clone were used to generate A23 transgenic mice [2].
• The A1-A23 sequence of NSc DS.PG (major fraction, C): NH2Asp-Glu-Ala-O-Gly-Ile-Gly-Pro-Glu-Val-Pro-Asp-Asp-Arg-Asp-Phe-G lu-Pro- Ser-Leu-Gly-Pro-Val was the same as reported for a DS.PG isolated from human fetal membrane (HFM) tissue (Brennan et al., 1984) [16].

Associations of IGKV2-24 with chemical compounds

• Thrombin-pretreated platelets will not retract a thrombin-induced fibrin clot unless ADP, sodium arachidonate, the ionophore A23, 187 or collagen are added together with thrombin [17].
• Collagen, arachidonate, thrombin, immune serum globulin, the ionophore A23, 187 and phytohaemagglutinin from Phaseolus vulgaris caused aggregation and release of granule contents [18].
• Calcineurin was inhibited by tyrphostins A8 (also designated AG10), A23 (AG18), and A48 (AG112) with p-nitrophenyl phosphate as substrate [19].
• Unlike Ca2+, Mn2+ could substitute for Mg2+, before and after addition of A23, showing its ability to regulate phosphorylation and succinate dehydrogenase activities, with almost the same efficiency as Mg2+ [20].
• Ionophores selective for Na+ (monensin, dianemycin), for K+ (valinomycin, nigericin), for Ca2+ (A23 187, X-537A), the calcium deregulatory substances amiprophosmethyl, fluphenazine, caffeine and the chelator EGTA have been applied to intact slime-producing root tips [21].

Other interactions of IGKV2-24

• CONCLUSIONS: The study strongly suggests the association among DR2, A23 and B21 allele and the evolution of ON to MS [22].

Analytical, diagnostic and therapeutic context of IGKV2-24

• Binding characteristics to 20K-, 22K-hGH and monkey GH (mGH) of these five mAbs, designated A23, B13, C02, D05, and D14, were analyzed by enzyme immunoassays (EIAs) and surface plasmon resonance analysis [23].
• Fifty pregnancy alloantisera directed towards HLA-A23 and/or A24 antigens were investigated serologically in titration studies against the three sequenced HLA-A9 specificities, A23 (A*2301), A24 (A*2402) and A2403 (A*2403) [24].

References