Disease relevance of ZNF382

• Monoclonal antibody KS1/4 recognizes an epitope expressed on the cell surface of human adenocarcinoma cells and certain epithelia [1].
• Phase I clinical comparative study of monoclonal antibody KS1/4 and KS1/4-methotrexate immunconjugate in patients with non-small cell lung carcinoma [2].
• The mAb KS1/4 recognizes a novel cell surface glycoprotein on a variety of epithelial carcinomas which may be a useful target Ag for antibody-directed diagnostic and therapeutic approaches [3].
• Real-time reverse transcription-PCR detects KS1/4 mRNA in mediastinal lymph nodes from patients with non-small cell lung cancer [4].
• The KS1/4 antibody reacts with a 40-kDa cell-surface glycoprotein antigen that is expressed on the surface of a variety of adenocarcinoma cells, including ovarian carcinoma [5].

High impact information on ZNF382

• KS1 contains 10 C2H2 zinc fingers, a KRAB-A/B motif, and an ID sequence that has been shown previously to participate in growth factor-regulated gene expression [6].
• Additional biochemical assays demonstrate that the KS1 KRAB domain interacts with the KAP-1 corepressor, and mutations that abolish this interaction alleviate KS1-mediated transcriptional repression [7].
• Reporter assays demonstrate that KS1 represses the expression of promoters containing this DNA sequence [7].
• Similarly, competitive binding studies between MAbs 17-1A and KS1/4 and MAb D612 revealed no similarity between the epitopes recognized by MAb D612 and MAbs 17-1A and KS1/4 [8].
• The human immune response to KS1/4-desacetylvinblastine (LY256787) and KS1/4-desacetylvinblastine hydrazide (LY203728) in single and multiple dose clinical studies [9].

Biological context of ZNF382

• Expression of a novel Krüpple-like zinc-finger gene, ZNF382, in human heart [10].
• The ZNF382 gene is mapped to chromosome 19q13.13 [10].
• With the aim of identifying genes involved in human heart development and disease, we have isolated a novel KRAB-related zinc-finger gene named ZNF382 from heart cDNA library [10].
• The ZNF382 gene has a predicted 548-amino acid open reading frame, encoding a putative 64kDa zinc-finger protein [10].
• Northern blot analysis indicates that a 2.9-kb transcript specific for ZNF382 is expressed at very early embryonic stage of human (at least earlier than gestation 34 day) and widely in human embryo tissues [10].

Anatomical context of ZNF382

• METHODS AND MATERIALS: CNE-1, CNE-2Z, and a normal human nasopharyngeal fibroblast strain, KS1, were infected with 2- and 6-plaque-forming units (pfu)/cell of Ad5CMV-p53, respectively [11].
• Cytogenetic analysis was performed on a cell line, designated KS1, derived from a Krukenberg tumor [12].
• Two transcript variants involving exon 7 were detected in K562 cells by RT-PCR, distinguishable from the wild-type transcript by deletions of 625 bp (KS32) and 988 bp (KS1) [13].

Associations of ZNF382 with chemical compounds

• It is proposed that in these mutants the first step in erythromycin biosynthesis is the charging of KS1 with propionate directly from propionyl-CoA [14].
• It has been most extensively demonstrated using a KS1 null mutation (KS1(0)) to block the first round of condensation in the biosynthesis of the erythromycin polyketide synthase (DEBS) for the production of analogues of its aglycone, 6-deoxyerythronolide B (6-dEB) [15].

Analytical, diagnostic and therapeutic context of ZNF382

• Deletion and site-directed mutagenesis reveal that KS1 requires nine C-terminal zinc fingers and the KRAB domain for transcriptional repression through the KBE site, whereas the isolated zinc finger and linker region are dispensable for this function [7].
• Western blotting analyses of tumor cell extracts utilizing KS1/4 reveal staining of a major Mr 40,000 band and a minor Mr 42,000 band [1].
• Digestion of the KS1/4 immunoprecipitates with neuraminidase prior to two-dimensional analysis or immunoprecipitation of short pulse-labeled extracts reduces the number of spots to three each at the Mr 40,000 and Mr 42,000 positions [1].
• Sequence analysis of the 5' and 3' noncoding regions of the KS1/4 cDNA revealed homologies to known proto-oncogenes and inflammatory mediators [3].
• SAMPLES: Data came from a large-scale longitudinal study of children over KS1 (4-7 years) [16].

References