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1

Cytogenetic analysis of the chromosome regions which attach to the nuclear envelope

100%
Sharakhov I. V.
Cellular and Molecular Biology Letters
|
2000
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tom 05
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nr 2
2

Potential suppressor gene loci and human prostate neoplasms

100%
Brys M., Krajewska W. M.
Cellular and Molecular Biology Letters
|
1997
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tom 02
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nr 4
The biology of prostate cancer is still poorly understood. Allelic loss studies indicate that there likely exist multiple sites harbouring candidate tumour suppressor genes (TSG), some of which may have an important role in primary tumours, and some in late stages of prostate cancer. The recent studies on the localization of potential TSG in neoplastic transformation of prostate comprise chromosome regions 7q, 8p, l0p/q, 16q, 17q, and 18q. In connection with accumulation of genetic changes affecting functioning of critical TSG, the multistep cancer progression hypothesis is a useful starting point in efforts to understand the biology of the neoplastic lesions of prostate.
3

Microdissected bovine X chromosome segment delineates homologous chromosomal regions in sheep and goat

84%
Bugno M., Zyga A., Slota E.
Folia Biologica
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2008
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tom 56
|
nr 3-4
149-151
4
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Molecular versus classical cytogenetics - evaluation of 20 Prader-Willi syndrome patients

84%
Stankiewicz P., Lebiocka J., Szpecht-Potocka A., Bocian E., Stanczak H., Obersztyn E., Mazurczak T.
Journal of Applied Genetics
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1997
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tom 38
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nr 2
Prader-Willi syndrome (PWS) is a developmental disorder caused by a deficiency of paternal contribution of the chromosome region 15q11.2-q13 arising from differently sized deletions, maternal disomy, or rarely imprinting mutations. We have analyzed 20 PWS patients using combined cytogenetic high resolution technique (HRT), fluorescence in situ hybridization (FISH) and molecular studies to identify parental origin (uniparental disomy) or molecular defect (deletion) of the Prader-Willi region. Lack of a paternal copy of 15q11.2-q13 resulting from its deletion was found in 16 patients. Using high resolution GTG banding on prometaphase chromosomes, deletion in the 15q11.2-q13 region was detected in only 8 patients. Application of FISH with different sets of PWS specific unique sequence probes (D15S11, SNRPN, D15S10, GABRß3) revealed microdeletions in 12 patients. In 12 out of 20 cases FISH confirmed HRT studies, while in 8 cases inconsistent results were obtained. No discrepancies between results of FISH and molecular studies were found, although the latter had a higher sensitivity. We conclude that FISH appears to be a rapid and reliable method of microdeletion identification and should be performed as a method of choice in cytogenetic diagnosis of Prader-Willi syndrome.
5

Direct interaction of Gas41 and Myc encoded by amplified genes in nervous system tumours

67%
Piccinni E., Chelstowska A., Hanus J., Widlak P., Loreti S., Tata A. M., Augusti-Tocco G., Bianchi M. M., Negri R.
Acta Biochimica Polonica
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2011
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tom 58
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nr 4
In order to understand better the role of the human Tip60 complex component Gas41, we analysed its expression levels in brain tumours and searched for possible interactors. Two-hybrid screening of a human foetal brain library allowed identification of some molecular interactors of Gas41. Among them we found n-Myc transcription factor. The interaction between Gas41 and n-Myc was validated by pull-down experiments. We showed that Gas41 is able to bind both n-Myc and c-Myc proteins, and that the levels of expression of Gas41 and Myc proteins were similar to each other in such brain tumors as neuroblastomas and glioblastomas. Finally, in order to identify which region of Gas41 is involved in the interaction with Myc proteins, we analysed the ability of Gas41 to substitute for its orthologue Yaf9 in yeast; we showed that the N-terminal portions of the two proteins, containing the YEATS domains, are interchangeable, while the C-terminal portions are species-specific. In fact we found that Gas41 C-terminal portion is required for Myc protein interaction in human.
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