Key Spec Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|H, M||WB, ICC, ELISA||Rb||Purified||Polyclonal Antibody|
|Presentation||Purified rabbit polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide.|
|Safety Information according to GHS|
|Material Size||100 µg|
|Anti-JMJD1B (N-terminus) - 1959695||1959695|
|Anti-JMJD1B (N-terminus) - NG1594520||NG1594520|
|Reference overview||Pub Med ID|
|Identification and characterization of TRIP8 gene in silico.|
Katoh, Masuko and Katoh, Masaru
Int. J. Mol. Med., 12: 817-21 (2003) 2003
TRIP1-TRIP15 genes encode thyroid hormone receptor beta (TR beta)-binding proteins. TRIP10 gene encodes FNBP1 family protein with FCH, FBH, and SH3 domains. Among 15 TRIP genes, TRIP8 gene remained uncharacterized except TRIP8 partial cDNA (L40411). Here, we determined the complete coding sequence of TRIP8 gene by using bio-informatics. Nucleotide sequence of full-length TRIP8 cDNA was determined in silico by assembling nucleotide sequences of FLJ14374 and DKFZp761F0118 cDNAs. TRIP8 protein (2540 aa) was found to consist of two bipartite nuclear localization signals (codon 352-368 and 2365-2381), TRI8H1 domain (codon 1697-1873), TRI8H2 domain (codon 2057-2351), and JMJC domain (codon 2387-2486). TRI8H1, TRI8H2 and JMJC domains were conserved among TRIP8, 5qNCA (C5orf7) and TSGA proteins. TR beta-binding domain was overlapped with N-terminal part of TRI8H2 domain, and C2HC4-type zinc finger-like motif was located within C-terminal part of TRI8H1 domain. Because JMJC domain proteins are implicated in chromatin remodeling, TRIP8 was predicted to be a transcriptional regulator associated with nuclear hormone receptors. Human TRIP8 gene, consisting of 26 exons, was about 300 kb in size. Intra-species comparative genomics revealed that TRIP8-EGR2 locus at human chromosome 10q21.3 and 5qNCA-EGR1 locus at human chromosome 5q31 are paralogous regions within human genome. Microsatellite marker D10S1225, associated with Alzheimer's disease, non-syndromic congenital retinal non-attachment (NCRNA) and non-syndromic autosomal recessive persistent hyperplastic primary vitreous (arPHPV), was located within the TRIP8-EGR2 locus. This is the first report on comprehensive characterization of the TRIP8 gene.
|A novel nuclear protein, 5qNCA (LOC51780) is a candidate for the myeloid leukemia tumor suppressor gene on chromosome 5 band q31.|
Hu, Z, et al.
Oncogene, 20: 6946-54 (2001) 2001
Interstitial deletion or loss of chromosome 5, del(5q) or -5, is a frequent finding in myeloid leukemias and myelodysplasias, suggesting the presence of a tumor suppressor gene within the deleted region. In our search for this gene, we identified a candidate, 5qNCA (LOC51780), which lies within a consistently-deleted segment of 5q31. 5qNCA expresses a 7.2-kb transcript with a 5286-bp open reading frame which is present at high levels in heart, skeletal muscle, kidney, placenta, and liver as well as CD34+ cells and AML cell lines. 5qNCA encodes a 191-kD nuclear protein which contains a highly-conserved C-terminus containing a zinc finger with the unique spacing Cys-X2-Cys-X7-His-X2-Cys-X2-Cys-X4-Cys-X2-Cys and a jmjC domain, which is often found in proteins that regulate chromatin remodeling. Expression of 5qNCA in a del(5q) cell line results in suppression of clonogenic growth. Preliminary sequence results in AML and MDS samples and cell lines has revealed a possible mutation in the KG-1 cell line resulting in a THR to ALA substitution that has not been found in over 100 normal alleles to date. We propose 5qNCA is a good candidate for the del(5q) tumor suppressor gene based on its predicted function and growth suppressive activities, and suggest that further mutational and functional study of this interesting gene is warranted.
|Transcript map and comparative analysis of the 1.5-Mb commonly deleted segment of human 5q31 in malignant myeloid diseases with a del(5q).|
Lai, F, et al.
Genomics, 71: 235-45 (2001) 2001
Loss of a whole chromosome 5, or a del(5q), are recurring abnormalities in malignant myeloid diseases. In previous studies, we defined a commonly deleted segment (CDS) of 1.5 Mb between D5S479 and D5S500 in patients with a del(5q), and we established a P1 artificial chromosome-based contig encompassing this interval. To identify candidate tumor suppressor genes (TSGs), we developed a transcript map of the CDS. The map contains 18 genes and 12 expressed sequence tags/UniGenes. Among the 18 genes are 10 genes that were previously cloned and 8 novel genes. The newly identified genes include CDC23, which encodes a component of the anaphase-promoting complex; RAB6KIFL, which encodes a kinesin-like protein involved in organelle transport; and KLHL3, which encodes a human homologue of the Drosophila ring canal protein, kelch. We determined the intron/exon organization of 14 genes and eliminated each gene as a classical TSG by mutation analysis. In addition, we established a single-nucleotide polymorphism map as well as a map of the mouse genome that is syntenic to the CDS of human 5q31. The development of a transcription map will facilitate the molecular cloning of a myeloid leukemia suppressor gene on 5q.
|Shotgun sequencing of the human transcriptome with ORF expressed sequence tags.|
Dias Neto, E, et al.
Proc. Natl. Acad. Sci. U.S.A., 97: 3491-6 (2000) 2000
Theoretical considerations predict that amplification of expressed gene transcripts by reverse transcription-PCR using arbitrarily chosen primers will result in the preferential amplification of the central portion of the transcript. Systematic, high-throughput sequencing of such products would result in an expressed sequence tag (EST) database consisting of central, generally coding regions of expressed genes. Such a database would add significant value to existing public EST databases, which consist mostly of sequences derived from the extremities of cDNAs, and facilitate the construction of contigs of transcript sequences. We tested our predictions, creating a database of 10,000 sequences from human breast tumors. The data confirmed the central distribution of the sequences, the significant normalization of the sequence population, the frequent extension of contigs composed of existing human ESTs, and the identification of a series of potentially important homologues of known genes. This approach should make a significant contribution to the early identification of important human genes, the deciphering of the draft human genome sequence currently being compiled, and the shotgun sequencing of the human transcriptome.
|cDNA cloning and genomic structure of three genes localized to human chromosome band 5q31 encoding potential nuclear proteins.|
Lai, F, et al.
Genomics, 70: 123-30 (2000) 2000
Loss of a whole chromosome 5, or a del(5q), is a recurring abnormality in malignant myeloid diseases. By cytogenetic and molecular analyses, we delineated previously a 1- to 1.5-Mb region that is deleted in all patients with a del(5q). In our efforts to identify a myeloid tumor suppressor gene within the commonly deleted segment (CDS), we have cloned and characterized the genes encoding three putative nuclear proteins, each of which contains a bipartite nuclear localization signal (NLS). In addition, C5ORF5 contains a putative rhoGAP domain at the N-terminus, C5ORF6 has a proline-rich sequence near the N-terminus, and C5ORF7 has a zinc-finger domain that partially overlaps the NLS. All three genes are ubiquitously expressed and encode novel proteins. The C5ORF5 cDNA is 5.47 kb encoding a protein of 915 amino acids (aa) with a predicted molecular mass of approximately 105 kDa. C5ORF5 has 23 exons spanning over 27 kb. The C5ORF6 transcript is 4.1 kb encoding a protein of 392 aa with a predicted molecular mass of approximately 43 kDa. C5ORF6 has 5 exons and spans approximately 11 kb. The C5ORF7 cDNA is 6.3 kb and encodes a protein of 1417 aa with a predicted molecular mass of approximately 155 kDa. C5ORF7 has 24 exons spanning approximately 64 kb. All three genes were localized to the distal half of the CDS between D5S1983 and D5S500. We evaluated each as a candidate tumor suppressor gene by the analysis of myeloid leukemia cells from patients with -5/del(5q), but no inactivating mutations were identified.