Disease relevance of IGKV1D-43

• Ribosomal proteins S13 and L23 promote multidrug resistance in gastric cancer cells by suppressing drug-induced apoptosis [1].
• A cDNA library specific for mRNA over-expressed in prostate cancer was generated by subtractive hybridization of transcripts originating from prostatic hyperplasia and cancer tissues. cDNA encoding ribosomal proteins L4, L5, L7a, L23a, L30, L37, S14 and S18 was found to be present among 100 analyzed clones [2].
• The effects of dipyridamole on MTA growth inhibition and end product reversal by thymidine and hypoxanthine was investigated in two lung cancer cell lines with (A549) and without (COR L23) dipyridamole-sensitive hypoxanthine rescue [3].
• BACKGROUND: This study was undertaken to characterize the two porcine lymphoblastoid cell lines L23 and L35, derived from a pig inoculated by the retrovirus Tsukuba-1, and to determine how they induce a strong human lymphocyte proliferation [4].
• The sarcoma showed a stemline with the same 7q-marker as L23 plus a marker del (12)(q13-24) [5].

High impact information on IGKV1D-43

• The molecular details of TFa interactions reveal that L23 is essential for the association of TF with the ribosome and may serve as a channel of communication with the nascent chain progressing in the tunnel [6].
• The interaction of L23 with MDM2 was enhanced by treatment with actinomycin D but not by gamma-irradiation, leading to p53 activation [7].
• L23 interacted with MDM2, forming a complex independent of the 80S ribosome and polysome [7].
• Cisplatin accumulation was unchanged in H69/CPR, 1.3-fold reduced in L23/CPR, and 2.0-fold reduced in MOR/CPR compared with their respective parent lines [8].
• Mutations of L23 reduced NAC ribosome binding in vivo and in vitro, whereas other eukaryotic ribosome-associated factors such as the Hsp70/40 chaperones Ssb or Zuotin were unaffected [9].

Chemical compound and disease context of IGKV1D-43

• METHODS: Chemosensitivity of the human adenocarcinoma cell line MOR/P and the cisplatin-resistant subline MOR/CPR as well as the large-cell lung cancer cell line L23/P and its cisplatin-resistant counterpart L23/CPR were evaluated by the MTT colorimetric assay [10].

Biological context of IGKV1D-43

• Moreover, transient transfection of the porcine B-cell line L23 showed up to 90% suppression of constitutive SLA-DR and SLA-DQ antigen expression in 5-8 days [11].
• Peptides containing single glycine, serine, alanine, or threonine amino acid substitutions at the buried L9, L16, L23, and I26 hydrophobic core positions of a GCN4-based sequence were synthesized and studied by solution-phase and crystallographic techniques [12].
• In addition, three ribosomal pseudogenes, L23a, S9, and L3, and some cDNAs with ESTs were mapped in the sequence [13].
• The IC50 values for MTA-induced growth inhibition were 28 and 640 nmol/L for COR L23 and A549 cells, respectively [3].
• The alignment of the amino acid sequence deduced from this gene with other proteins revealed that this protein is related to the L23/25 rihosomal protein family [14].

Anatomical context of IGKV1D-43

• L23 and L24, on the other hand, existed on approximately two-third of B cells in blood and lymphoid tissues [15].
• These L23 and L24 antigens were expressed largely on small lymphocytes located in the mantle zone of lymphoid follicles and to a lesser extent on large blastic cells within lymphoid germinal centers [15].
• Furthermore, L23a- and S14-transcript levels were significantly elevated in PC-3 cells as compared with those in the normal prostate epithelial cell line PrEC [2].
• Prevention of MTA growth inhibition by thymidine and/or hypoxanthine was investigated in two human lung (A549, COR L23) and two breast (MCF7, T47D) tumour cell lines, and the effect of the nucleoside/base transport inhibitor dipyridamole (DP) on thymidine and hypoxanthine rescue defined [16].
• This mutated CIITA (mCIITA) was able to repress DR and DQ expression in 45.0-60.0% of the mCIITA-transfected clones of swine endothelial cell line PIEC and in B cell line L23, as well as in human cell lines HeLa and Raji [17].

Associations of IGKV1D-43 with chemical compounds

• We conclude that NAC employs a conserved ribosome binding domain to position itself on the L23 ribosomal protein adjacent to the nascent polypeptide exit site [9].
• Immunoprecipitation studies showed that L23 and L24 were different molecular species consisting of a single glycoprotein with m.w. of 205,000 and 145,000, respectively [15].
• Dipyridamole blocked the partial rescue from MTA-induced growth inhibition by thymidine alone as well as the complete rescue by thymidine plus hypoxanthine not only in A549 cells, which have dipyridamole-sensitive hypoxanthine transport, but also in COR L23 cells, in which hypoxanthine uptake is insensitive to dipyridamole [3].
• In growth inhibition assays MRP-over-expressing COR L23/R cells were 20 times more resistant to VP16 and doxorubicin compared with the parental COR L23/R human lung carcinoma cells [18].
• Tyrphostins B46 [N-(3-phenylpropyl)-3,4-dihydroxybenzylidene cyanoacetamide] and B56 (both highly protein-bound) inhibited DNA synthesis of L23/P cells with approximately 3-fold greater potency in 0.5% serum than in 10% serum, but the inhibition of DNA synthesis in 0.5% serum was reduced by the addition of BSA [19].

Analytical, diagnostic and therapeutic context of IGKV1D-43

• Whereas H69/CPR and MOR/CPR showed little or no cross-resistance to any of the other compounds, L23/CPR was generally cross-resistant to all of them [8].
• Twenty-one patients received a single epidural injection of 20 ml 0.5% bupivacaine at the L23 or L34 interspace and 23 patients received 20 ml 0.75% ropivacaine in a similar manner [20].

References