Disease relevance of IGKV2-30

• METHODS: Priming of blood eosinophils obtained from patients with allergy and donors without allergy was measured by labeling with monoclonal phage antibodies A17 and A27 recognizing priming-associated epitopes on phagocytes [1].
• F10 localized predominantly in the cortical region of immature virions, beneath the membrane where A17 is located [2].
• In addition, CAP and UC781 had complementary effects against HIV-1 infection since (i) CAP inhibited infection by the UC781-resistant strain HIV-1(IIIB) A17 and (ii) pretreatment of MT-2 cells with UC781, but not CAP, abolished subsequent infection after removal of the compound [3].
• Michellamine B was active against a panel of biologically diverse laboratory and clinical strains of HIV-1, including the AZT-resistant strain G910-6 and the pyridinone-resistant strain A17; the compound also inhibited several strains of HIV-2 [4].
• The NOE distance constraints establish that the glycosidic torsion angle is syn at (AF)G6 and anti at A17, which results in the aminofluorene ring being positioned in the minor groove [5].

Psychiatry related information on IGKV2-30

• Nevertheless, EL like illness has never been reported in Thailand. A 17 year-old man presented with hypersomnolence one week before admission [6].

High impact information on IGKV2-30

• In particular, cases expressing stereotyped IGHV4-39/IGKV1-39-1D-39 and IGHV4-34/IGKV2-30 were always IgG-switched [7].
• Furthermore, A30 and G7 stimulated F10-dependent phosphorylation of A17 in the absence of other viral late proteins [2].
• Further analyses demonstrated that tyrosine and threonine phosphorylation of the A17 membrane component was inhibited in the absence of inducer [8].
• The processing of core proteins is coupled to morphogenesis and is inhibited by the drug rifampin, whereas processing of the A17 membrane protein occurs at an earlier stage of assembly and is unaffected by the drug [9].
• RNase protection experiments agreed with the molecular modeling studies which suggested that the ethidium moiety of 20 was inserted next to the A17 residue while the arginine side chain occupied the pyrimidine bulge [10].

Chemical compound and disease context of IGKV2-30

• Notably, the lead fluorothiourea compounds 11 and 12 were both substantially more active against the NNRTI-resistant HIV strains RT-MDR (V106A) and A17 (Y181C) than nevirapine or delavirdine [11].
• HI-511 R inhibited the HIV-strain A17 variant, containing RT mutations Y181C plus K103N, with an IC50 value of 2.7 microM, whereas the IC50 values of nevirapine, delavirdine, and trovirdine against this highly NNI-resistant HIV-1 strain were >100 microM [12].
• Significant improvements compared to lopinavir were seen in cell culture activity versus wild-type virus (pNL4-3) and the lopinavir-resistant mutant virus A17 (generated by in vitro serial passage of HIV-1 (pNL4-3) in MT-4 cells) [13].

Biological context of IGKV2-30

• However, tyrosine phosphorylation and proteolytic cleavage of the A17 membrane protein and proteolytic cleavage of core proteins were inhibited at 40 degrees C, suggesting an assembly defect [14].
• Two antibody clones with unique amino acid sequences could be readily purified, and the sequences of their light chains match those of A1/A17 V kappa and hslv2046 V lambda genes [15].
• We also studied the presence and distribution of MtRs in Medicago accession R108-1, a genotype with a genome that is 20% smaller than that of Jemalong A17 [16].
• We searched for such repeats in the functional centromeres of the model legume Medicago truncatula (Medicago) accession Jemalong A17 [16].
• In vitro stimulation of eosinophils with cytokines leads to up-regulation of CD11b and priming markers recognized by the recently developed priming markers A17 and A27, whereas interleukin (IL)-5Ralpha is being down-regulated [17].

Anatomical context of IGKV2-30

• Concentrations of immunoreactive somatostatin-28(1-12) were significantly increased in the caudate and putamen but were unchanged in cortical areas A9 and A17 [18].
• By Northern blot hybridization, SALS was associated with increased mRNA for C1qB and clusterin in the motor cortex (Brodmann area A4), but not in superior temporal cortex (A17), relative to neurologically normal controls [19].
• Modulation of the leukocyte compartment as a consequence of systemic activation by cytokines/chemokines was determined by measuring the expression of priming-associated epitopes by novel antibodies designated A17 and A27 [20].
• The slow GABA(C)Rs truncated glutamate release, making the A17 amacrine cell L-EPSCs more transient, whereas the fast GABA(A)R and glycineRs reduced the initial phase of glutamate release, limiting the peak amplitude of the L-EPSC [21].
• In the adult cat, axons running through the corpus callosum interconnect the border between the visual cortical areas 17 and 18 (A17 and A18) of both hemispheres [22].

Associations of IGKV2-30 with chemical compounds

• The unpaired A17 residue delimits a small cavity which constitutes a receptor site for small molecules, especially for ethidium bromide [10].
• Although basal A17 and A27 expression was not increased, we observed a significantly higher expression of these priming epitopes on N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated cells of RSV patients compared with cells of controls, indicative of prior in vivo priming [17].
• Presently kappa-OR mRNA expression was studied in different cortical areas (A4, A10, A17) by in situ hybridization using digoxigenin-labeled oligonucleotides and an alkaline phosphatase-mediated color reaction. kappa-OR mRNA was expressed mainly in layers II/III and V pyramidal and layer VI multiform neurons [23].
• Postmortem membrane receptor binding for markers within the phosphoinositide (PI) system showed that TS samples had increased [3H]phorbol ester binding to protein kinase C sites in area A17, but normal binding in A4 [24].
• The activity of HI-443 against A17 was ten times more potent than that of trovirdine, 2083 times more potent than that of nevirapine, and 1042 times more potent than that of delavirdine [25].

Analytical, diagnostic and therapeutic context of IGKV2-30

• Direct sequence analysis of the PCR products revealed that, except for a number of silent mutations, the single rearranged VK gene was identical to the germline A1-A17 VK gene [26].
• In a second approach, microarray analysis was used to compare levels of alfalfa transcripts corresponding to 16,086 Medicago truncatula A17 genes in stems with and without trichomes [27].
• An ELISA was developed with a purified mixture of A17 and VacA antigens to test the different groups of patients [28].
• Negative-ion HPLC/PDA/ESI/MS and HPLC/PDA/ESI/MS/MS spectra were utilized along with HPLC retention times to profile and identify 27 saponins in M. truncatula (cultivar Jemalong, A17) [29].
• Immunoblotting located the A17 antibody on CNBr fragment 4 of apo A-I and the A30 antibody on CNBr fragment 1 [30].

References