A new DNA binding and dimerization motif in immunoglobulin enhancer binding, daughterless, MyoD, and myc proteins

Murre, Cornelis; McCaw, Patrick Schonleber; Baltimore, David

doi:10.1016/0092-8674(89)90682-x

Cited by 2,544 publications

(1,835 citation statements)

References 29 publications

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“…If these 2 microsatellites were homozygous, we considered the results of the 2 other microsatellites (D7S2559 and D7S2532). D7S2559 or D7S2532 differed from the other markers in 9 tumors (patients 6,8,11,15,33,59, 68, 70, and 73). Then, the results of D7S2559 and D7S2532 microsatellites help to define the possible limits of 7p21 locus abnormalities: D7S2559 or D7S2532 showed FIGURE 1 -AI.…”

Section: The Twist Locus Seems To Be Frequently Implicated In Pediatrmentioning

confidence: 80%

“…2 Classic genetics and molecular embryology originally established that the functions of its orthologous twist (in Drosophila) and homologous M-twist (in Mus) genes, which were shown to be indispensable at early embryonic developmental stages, 3,4 encode a B-HLH transcription factor, [5][6][7] which contains a histone acetyl transferase (HAT)-binding domain. 8 Heterozygosity at TWIST resulting in haploinsufficiency has been shown to alter bone differentiation in human patients presenting with Saethre-Chotzen diagnosis.…”

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confidence: 99%

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Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas

Entz‐Werlé

Stoetzel

Berard-Marec

et al. 2005

Intl Journal of Cancer

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The identification of genes as markers for chromosome aberrations in specific tumors might facilitate oncogenesis mechanism comprehension, cancer detection, prediction of clinical outcomes, and response to therapy. Previous physiologic and oncologic data identified the TWIST gene as a marker for mesodermal derivative and bone tissue differentiation, but its contribution to bone malignancies has not been investigated. In the present study, search for genomic alterations in high-grade pediatric osteosarcomas was focused on the 7p21 region, and more specifically on the TWIST gene. In a cohort of 74 patients, we observed by allelotyping that 31 of 68 informative tumors were rearranged at the TWIST locus. Among them, analysis by quantitative PCR (QPCR) revealed that, surprisingly, mostly deletions (22/68), but also amplifications (9/ 68), of the TWIST gene were detected. Furthermore, deletions at TWIST were statistically correlated to other molecular abnormalities, like alterations at the APC or c-kit loci, as well as to clinical features such as a poor outcome. This work shows that the TWIST gene seemed to be involved in high-grade pediatric osteosarcomas and is a new marker with a possible initial predictive value. ' 2005 Wiley-Liss, Inc.

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Section: The Twist Locus Seems To Be Frequently Implicated In Pediatrmentioning

confidence: 80%

mentioning

confidence: 99%

Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas

Entz‐Werlé

Stoetzel

Berard-Marec

et al. 2005

Intl Journal of Cancer

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“…Similar to all seven classes of the HLH family of transcription factors (Atchley and Fitch, 1997;Massari and Murre, 2000), the Id HLH motif allows Ids to form heterodimers with class I (E proteins), and some class II proteins (MyoD, myogenin, Myf5, Myf6;(Murre et al, 1989a). However, while all other HLH classes contain a basic DNA-binding domain at the N-terminus (hence, the designation 'bHLH') and bind consensus E-box (CANNTG), or N box (CACNAG) DNA sequences (Murre et al, 1989b;Murre et al, 1994) found in regulatory regions of many genes involved in growth, differentiation, and apoptosis, the Id proteins lack this basic region, acting as DN inhibitors of class I and II proteins.…”

Section: Introductionmentioning

confidence: 99%

Id3 induces a caspase-3- and -9-dependent apoptosis and mediates UVB sensitization of HPV16 E6/7 immortalized human keratinocytes

et al. 2006

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Inhibitor of differentiation/DNA binding (Id) proteins comprise a class of helix-loop-helix transcription factors involved in proliferation, differentiation, apoptosis, and carcinogenesis. We have shown that while Id2 is induced by UVB in primary keratinocytes, Id3 is upregulated only in immortalized cells. We have now determined that the consequences of ectopic expression of Id3 protein are strikingly different between immortalized and primary keratinocytes. Overexpression of Id3 induces a significant increase in apoptotic cells as revealed by Annexin V positivity as well as proteolytic processing of caspase-3 in immortalized, but not in primary keratinocytes. Id3-green fluorescent protein (GFP)-positive cells exhibited a fivefold increase in apoptotic nuclear fragmentation compared to Id3-GFP-negative cells. These apoptotic responses were accompanied by activation of caspase-3, as shown by immunocytochemical staining with antibodies to active caspase-3. Immunostaining with antibodies to the active form of caspase-9 as well as to the active form of Bax further revealed that induction of apoptosis in Id3-overexpressing keratinocytes occurred via a mitochondrial-caspase-9-mediated pathway. Coexpression of dominant-negative caspase-9 with Id3 significantly suppressed apoptotic nuclear fragmentation, indicating that caspase-9 activation is essential for Id3-induced cell death. This response was also markedly attenuated by coexpression with the Bax antagonist antiapoptotic protein Bcl2, confirming a role for Bax activation in this apoptotic response. Id3-induced Bax activation may result from increased expression of Bax protein. Furthermore, reduction of Id3 expression by small interfering RNAs abrogated the UVB-induced proteolytic activation of caspase-3 in these cells. These data together suggest that UVB-induced apoptosis of immortalized keratinocytes is at least in part due to Id3 upregulation in these cells.

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“…Table 1). Several of the known cDNAs, including c-fgr, E2A, osteonectin, mac25, and GAP SH3 binding protein, have been reported to be involved in breast and other cancers (Abts et al, 1991;Murre et al, 1989;Shimasaki et al, 1991). One of the novel genes, Di12, was characterized in detail and RT ± PCR and immunohistochemistry were used to examine its potential as a tumor marker in breast malignancies.…”

Section: Discussionmentioning

confidence: 99%

Breast cancer genome anatomy: correlation of morphological changes in breast carcinomas with expression of the novel gene product Di12

Burger

Zhang

et al. 1998

Oncogene

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To determine which genes may be activated or inactivated during breast cancer development, we employed two cloning strategies (subtractive hybridization and di erential display) using RNA samples from a human breast tumor and its matching normal breast cell line. Of 950 clones isolated, 102 cDNA inserts were analysed by DNA sequencing and database searching. We found 30 clones that were obviously unidenti®ed, with no signi®cant homology to any listed human gene. We focused upon one of the novel genes, Di12, that is di erentially expressed as a 1.35 kb RNA in breast cancer tissues and cell-lines, and in several normal tissues. A full length cDNA of this gene was cloned, and its DNA sequence revealed an open reading frame of 339 amino acids. Antibodies to the ten N-terminal amino acids were developed to investigate the expression of Di12 in breast cancer cell-lines and tumors. The Di12 protein was found in tissue sections of in®ltrating ductal carcinomas (IDCs), but not in benign or normal breast specimens. RT ± PCR analysis con®rmed expression of Di12 in 80% of in®ltrating ductal carcinomas (IDCs). As IDC constitutes *70% of breast cancers seen clinically, the level of Di12 expression may be predictive of disease progression.

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A new DNA binding and dimerization motif in immunoglobulin enhancer binding, daughterless, MyoD, and myc proteins

Cited by 2,544 publications

References 29 publications

Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas

Frequent genomic abnormalities at TWIST in human pediatric osteosarcomas

Id3 induces a caspase-3- and -9-dependent apoptosis and mediates UVB sensitization of HPV16 E6/7 immortalized human keratinocytes

Breast cancer genome anatomy: correlation of morphological changes in breast carcinomas with expression of the novel gene product Di12

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