Genomic organization of a tumor growth inhibitor geneING1

Baranova, Anna; Ivanov, Dmitry; Makeeva, Natalia; Corcoran, Martin; Никитин, Е. А.; Borodina, Tatiana; Полтараус, А. Б.; Глинщикова, О А; Soudarikov, A. B.; Oscier, David; Yankovsky, N. K.

doi:10.1007/bf02759644

Cited by 2 publications

(3 citation statements)

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“…The difference in sequence from previous published data that we demonstrated has since been confirmed by other authors. (9,12) We conclude that mutation is likely to be an uncommon mechanism for alteration of ING1b in human tumors. Thus, we decided to investigate ING1b protein expression and subcellular localization, which might have bearing upon its function or the efficacy of its function.…”

Section: Discussionmentioning

confidence: 93%

“…Recent evidence has revealed the presence of distinct CpG islands flanking each of the three individual exons of ING1 suggesting that regulation of ING1 expression may also be mediated as a result of de novo DNA methylation. (9) Studies of the structure and function of the mouse ING1 gene have shown that the mouse ING1 gene encodes three differentially spliced transcripts. Two of these encode PHD finger proteins.…”

Section: Discussionmentioning

confidence: 99%

“…(4)(5)(6)(7)(8) ING1 has been found to encode a series of differentially spliced mRNAs, with variable initiation sites and usage of three distinct exons, which may be translated to produce a family of proteins p47 ING1a , p33 ING1b , p27, and p24 ING1e . (9)(10)(11)(12)(13) The most widely expressed of these protein isoforms, however, appears to be p33 ING1b . (14) The role of ING1 as a gene encoding chromatin remodelling proteins is supported by the study of Yng2 from S. cervisiae.…”

Section: Introductionmentioning

confidence: 99%

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Comparative Assessment Expression of the Inhibitor of Growth 1 Gene (ING1) in Normal and Neoplastic Tissues

Nouman

Angus²,

Lunec

et al. 2002

Hybridoma and Hybridomics

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Studies have indicated that the tumor suppressor p33(ING1b) (13q33-34) interact with p53. Moreover, the association of functional protein forms of each member of the p33(ING1b)/p53 complex is essential for optimum activity of p53. The present report describes the sequencing of cDNAs corresponding to the p33(ING1b) mRNAs in a series of normal and tumor cell lines, and the production of monoclonal antibodies (MAbs) reactive with p33(ING1b). These antibodies were subsequently used to analyze p33(ING1b) expression in normal and tumor cell lines and tissues. No evidence of mutation of p33(ING1b) was found in any of the 15 tumor cell lines cDNAs studied. Our investigation of a wide range of normal tissues have shown that expression of the nuclear epitope is highly ubiquitous, whereas expression of the cytoplasmic form could be detected in only 50% of tissues studied. Considering neoplastic tissues, loss of nuclear p33(ING1b) was observed in melanoma, seminoma, papillary thyroid carcinoma, ductal breast carcinoma, and acute lymphoblastic leukemia. As with normal tissue, cytoplasmic p33(ING1b) was more restricted, being observed in around 30% of neoplastic tissues, but in melanoma, papillary thyroid carcinoma, ductal breast carcinoma, there was increased detection of cytoplasmic p33(ING1b) associated with concomitant loss of nuclear expression. These results may suggest that at least in some tumors, loss of effective p33(ING1b) function may be achieved by translocation to the cytoplasm or failure of nuclear localization.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%