Disease relevance of IGKV1D-27

• Evidence suggests that generation of such fibrils may be involved in the etiology of this disease, since mutations in the coding region of the beta/A4 amyloid precursor protein (APP) gene segregate with familial cerebral amyloidoses, including familial Alzheimer's disease [1].
• Prognostic relevance of MAGE-A4 tumor antigen expression in transitional cell carcinoma of the urinary bladder: a tissue microarray study [2].
• Retinoic acid (RA) induced differentiation of SH-SY5Y neuroblastoma cells is associated with more than a tenfold induction of total Alzheimer's disease beta A4 amyloid protein precursor (APP) mRNA as analyzed by Northern blot hybridisation [3].
• While C-terminally truncated variants were shown to be present in normal body fluids, a single Glu-->Gln change in the 39 amino acid form of beta A4 results in accelerated fibril formation in the brains of patients with Dutch-type hereditary cerebral hemorrhage with amyloidosis [4].
• Four members of globomycin, SF-1902 A2, A3, A4a and A4b were newly isolated from the culture of Streptomyces hygroscopicus SF-1902 [5].

Psychiatry related information on IGKV1D-27

• Cerebral deposition of fibrils formed from the beta/A4 amyloid protein is an invariable feature of Alzheimer's disease [1].

High impact information on IGKV1D-27

• The effect of the A4 peptide on shear-induced platelet aggregation was accompanied by the attenuation of shear-induced filamin A binding to GpIbalpha and diminished shear-dependent protein tyrosine phosphorylation [6].
• This review examines the evidence regarding linkage disequilibrium and haplotype structure within the A1/C3/A4/A5 cluster, and assesses its association with plasma lipids and cardiovascular disease risk [7].
• The APOA1/C3/A4/A5 gene cluster, lipid metabolism and cardiovascular disease risk [7].
• In contrast to previous studies using histochemical methods, the authors observed large numbers of diffuse plaques in the AD hypothalamus labeled with an antiserum to the beta-amyloid, or A4 peptide, of the beta-amyloid precursor proteins (beta APPs), whereas A4-immunoreactive plaques were uncommon in the hypothalamus of patients without AD [8].
• The inducible expression of wild-type p53 and the A4 mutant in H1299 cells caused growth inhibition due to cell-cycle arrest [9].

Biological context of IGKV1D-27

• When the A4 peptide was delivered to intact human platelets using a carrier peptide, we observed the dose-dependent inhibition of VWF-induced platelet aggregation in response to both ristocetin and shear stress [6].
• Study of the sequence tagged site (STS) in the beginning of human apo A4 gene region [10].
• We analyzed 4 kb of the human HOX A4 gene promoter and identified seven putative AP-2-binding sites in the DNA sequence [11].
• In N-ras-transformed cells, low HOX A4 promoter activity results from ras inhibition of AP-2 transactivation [11].
• The results indicate that the combining site of these immunoglobulins shows highest complementarity for a trifructofuranosyl sequence (A4 and A47N) and a tetrafructofuranosyl sequence (U61 and E109) [12].

Anatomical context of IGKV1D-27

• We now report that some neurofibrillary tangles ('tombstone tangles') are also A4 immunoreactive [13].
• Soluble derivatives of beta/A4 amyloid protein precursor in human cerebrospinal fluid are both N- and O-glycosylated [14].
• Furthermore, in each case, greater quantities of beta A4 were observed in the frontal rather than the temporal lobes [15].
• We report here the identification of a new MAGE-A4 encoded peptide, which is recognized by a cytolytic T lymphocyte (CTL) clone on HLA-B*3701 [16].
• This observation is consistent with the hypothesis that A4 amyloid accumulation is a component of both neurofibrillary tangles and neuritic plaques [13].

Associations of IGKV1D-27 with chemical compounds

• The linkage of the glycan chain to the beta/A4 amyloid protein precursor (APP) in cerebrospinal fluid (CSF) was studied by Western blot analysis [14].
• With the onset of drought only A4 increased the xanthophyll cycle pool, F2000 remaining constant throughout the drought cycle [17].
• Contrarily, sucrose contents decreased with drought but the effects were larger in A4 than in F2000 [17].

Analytical, diagnostic and therapeutic context of IGKV1D-27

• Analysis of the A4 domain (C321S mutant) by size exclusion chromatography indicated the presence of a slowly equilibrating reversible monomer-dimer equilibrium [18].
• These data suggest that evaluation of MAGE-A4 protein expression is useful in the identification of groups of TCCs characterized by severe prognosis, thus possibly providing indications for early MAGE TAA-targeted immunotherapy [2].
• We have devised a sensitive method based on the polymerase chain reaction (PCR) to detect expression of human interferon-alpha-encoding genes (IFN-A) in general, and specifically, expression of the IFN-A2 or IFN-A4 genes [19].
• When tumor cells expressing MAGE-A4 were transfected with HLA-B*3701, they were recognized by the CTL clone, demonstrating that the peptide ought to be processed in tumor cells and could therefore serve as a target for therapeutic antitumoral vaccination [16].
• An S1 nuclease protection assay was designed to study the splicing pattern of the alternatively spliced beta A4 amyloid gene (APP gene) of Alzheimer's disease (AD) [20].

References