@article{HigginsSmilinichSaitetal.1994,
author = {Higgins, M. J. and Smilinich, N. J. and Sait, S. and Koenig, A. and Pongratz, J. and Gessler, Manfred and Richard III., C. W. and James, M. R. and Sanford, J. P. and Kim, B.-W. and Cattelane, J. and Nowak, N. J. and Winterpacht, A. and Zabel, B. U. and Munroe, D. J. and Bric, E. and Housman, D. E. and Jones, C. and Nakamura, Y. and Gerhard, D. S. and Shows, T. B.},
title = {An Ordered NotI Fragment Map of Human Chromosome Band 11p15},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-45766},
year = {1994},
abstract = {An ordered NotI fragment map containing over 60 loci and encompassing approximately 17 Mb has been constructed for human chromosome band llpl5. Forty-two probes, including 11 NotI-linking cosmids, were subregionaUy mapped to llpl5 using a subset of the Jl-deletion hybrids. These and 23 other probes defining loci previously mapped to 11p15 were hybridized to genomic DNA digested with NotI and 5 other infrequently cleaving restriction enzymes and separated by pulsed-field gel electrophoresis. Thirty-nine distinct NotI fragments were detected encompassing approximately 85\% of the estimated length of llp15. The predicted order of the gene loci used is cenMYODI- PTH-CALCA-ST5-RBTNI-HPX-HBB-RRMlTH/ INS!1GF2-H19-CTSD-MUC2-DRD4-HRAS-RNHtel. This map wiu allow higher resolution mapping of new Ilp15 markers, facilitate positional cloning of disease genes, and provide a framework for the physical mapping of llp15 in clone contigs.},
subject = {Genom / Genkartierung / Genanalyse},
language = {en}
}
@article{VortkampGesslerPaslieretal.1994,
author = {Vortkamp, Andrea and Gessler, Manfred and Paslier, D. Le and Elaswarapu, R. and Smith, S. and Grzeschik, Karl-Heinz},
title = {Isolation of a yeast artificial chromosome contig spanning the Greig cephalopolysyndactyly syndrome (GCPS) gene region},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-30182},
year = {1994},
abstract = {Disruption of the zinc finger gene GLI3 has been shown to be the cause of Greig cephalopolysyndactyly syndrome (GCPS), at least in some GCPS translocation patients. To characterize this genomic region on human chromosome 7p13, we have isolated a VAC contig of more than 1000 kb including the GLI3 gene. In this contig the gene itself spans at least 200-250 kb. A CpG island is located in the vicinity of the 5' region of the known GLI3 cDNA, implying a potential promoter region.},
language = {en}
}
@article{GesslerKoenigArdenetal.1994,
author = {Gessler, Manfred and K{\"o}nig, A. and Arden, K. and Grundy, P. and Orkin, S. H. and Sallan, S. and Peters, C. and Ruyle, S. and Mandell, J. and Li, F. and Cavenee, W. and Bruns, G. A.},
title = {Infrequent mutation of the WT1 gene in 77 Wilms' Tumors},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-34308},
year = {1994},
abstract = {Homozygous deletions in Wilms' tumor DNA have been a key step in the identification and isolation of the WTI gene. Several additional loci are also postulated to contribute to Wilms' tumor formation. To assess the frequency of WTI alterations we have analyzed the WTI locus in a panel of 77 Wilms' tumors. Eight tumors showed evidence for large deletions of several hundred or thousand kilobasepairs of DNA, some of which were also cytogenetically detected. Additional intragenic mutations were detected using more sensitive SSCP analyses to scan all 10 WTI exons. Most of these result in premature stop codons or missense mutations that inactivate the remaining WTI allele. The overall frequency of WTI alterations detected with these methods is less than 15\%. While some mutations may not be detectable with the methods employed, our results suggest that direct alterations of the WTI gene are present in only a small fraction of Wilms' tumors. Thus, mutations at other Wilms' tumor loci or disturbance of interactions between these genes likely play an important role in Wilms' tumor development.},
language = {en}
}
@article{GesslerKonigMooreetal.1993,
author = {Gessler, Manfred and Konig, Anja and Moore, Jay and Qualman, Steven and Arden, Karen and Cavenee, Webster and Bruns, Gail},
title = {Homozygous inactivation of WTI in a Wilms' tumor associated with the WAGR syndrome},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59146},
year = {1993},
abstract = {Wilms' tumor is a childhood nephroblastoma that is postulated to arise through the inactivation of a tumor suppressor gene by a two-hit mechanism. A candidate II p 13 Wilms' tumor gene, WTI, has been cloned and shown to encode a zinc finger protein. Patients with the WAGR syndrome (Wilms' tumor, aniridia, genitourinary abnormalities, and mental retardation) have a high risk of developing Wilms' tumor and they carry constitutional deletions of one chromosome II allele encompassing the WTI gene. Analysis of the remaining WTI allele in a Wilms' tumor from a WAGR patient revealed the deletion of a single nucleotide in exon 7. This mutation likely played a key role in tumor formation, as it prevents translation of the DNA-binding zinc finger domain that is essential for the function of the WTI polypeptide as a transcriptional regulator.},
subject = {Biochemie},
language = {en}
}
@article{HenryHooversBarichardetal.1993,
author = {Henry, Isabelle and Hoovers, Jan and Barichard, Fernande and Berth{\´e}as, Marie-Francoise and Puech, Anne and Prieur, Fabienne and Gessler, Manfred and Bruns, Gail and Mannens, Marcel and Junien, Claudine},
title = {Pericentric intrachromosomal insertion responsible for recurrence of del(11)(p13p14) in a family},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59157},
year = {1993},
abstract = {The combined use of qualitative and quantitative analysis of I I p I 3 polymorphic markers tagether with chromosomal in situ suppression hybridization (CISS) with biotin labeled probes mapping to I I p allowed us to characterize a complex rearrangement segregating in a family. We detected a pericentric intrachromosomal insertion responsible (or recurrence of del( I I )(p 13p 14) in the family: an insertion of band I I p 13-p 14 carrying the genes for predisposition to Wilms' tumor, WT I, and for aniridia, AN2, into the long arm of chromosome I I in II q 13-q 1<4. Asymptomatic balanced carriers were observed over three generations. Classical cytogenetics had failed to detect this anomaly in the balanced carriers, who were first considered to be somatic mosaics for del( II )(p 13). Two of these women gave birth to children carrying a deleted chromosome II. most likely resulting from the loss of the I I p 13 band inserted in I I q. Although in both cases the deletion encompassed exactly the same maternally inherited markers, there was a wide Variation in clinical expression. One child, with the karyotype 46,XY,del(ll)(pllpl4), presented the full-blown WAGR syndrome with anlridia, mental retardation, Wilms' tumor, and pseudohermaphroditism, but also had proteinuria and glomerular sclerosis reminiscent of Drash syndrome. In contrast, the other one, a girl with the karyotype 46,XX,del( I I )(p I 3), only had aniridia. Although a specific set of mutational sites has been observed in Drash patients, these findings suggest that the loss of one copy of the WTI gene can result in similar genital and kidney abnormalities.},
subject = {Biochemie},
language = {en}
}
@article{KonigJakubiczkaWieackeretal.1993,
author = {Konig, Anja and Jakubiczka, Sybille and Wieacker, Peter and Schl{\"o}sser, Hans W. and Gessler, Manfred},
title = {Further evidence that imbalance of WT1 isoforms may be involved in Denys-Drash syndrome},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59167},
year = {1993},
abstract = {No abstract available},
subject = {Biochemie},
language = {en}
}
@article{PoulatMorinKonigetal.1993,
author = {Poulat, F. and Morin, D. and Konig, A. and Brun, P. and Giltay, J. and Sultan, C. and Dumas, R. and Gessler, Manfred and Berta, P.},
title = {Distinct molecular origins for Denys-Drash and Frasier syndromes},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59172},
year = {1993},
abstract = {The direct involvment of the Wilm's tumor suppressor gene (WTl) in Denys-Drash syndrome through mutations within exons 8 or 9 has recently been established. The absence of such alterations in three patients with Frasier syndrome provides a molecular basis for distinguishing these two syndromes that are associated with streak gonads, pseudohermaphroditism and renal failure.},
subject = {Biochemie},
language = {en}
}
@article{GesslerGrupeGrzeschiketal.1992,
author = {Gessler, Manfred and Grupe, Andrew and Grzeschik, Karl-Heinz and Pongs, Olaf},
title = {The potassium channel gene HK1 maps to human chromosome 11p14.1, close to the FSHB gene},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59184},
year = {1992},
abstract = {Transiently activating (A-type) potassium (K) channels are important regulators of action potential and action potential firing frequencies. HK1 designates the firsthuman cDNA that is highly homologous to the rat RCK4 cDNA that codes for an A-type K-channel. The HK1 channel is expressed in heart. By somatic cell hybrid analysis, the HK1 gene has been assigned to human chromosome 11p13-pl4, the WAGR deletion region (Wilms tumor, aniridia, genito-urinary abnormalities and mental retardation). Subsequent pulsed field gel (PFG) analysis and comparison with the well-established PFG map of this region localized the gene to 11p14, 200-600 kb telomeric to the FSHB gene.},
subject = {Biochemie},
language = {en}
}
@article{GesslerKoenigBruns1992,
author = {Gessler, Manfred and K{\"o}nig, A. and Bruns, G. A. P.},
title = {The genomic organization and expression of the WT1 gene},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59195},
year = {1992},
abstract = {The Wilms tumor gene WTl, a proposed tumor suppressor gene, has been identifled based on its location within a homozygous deletion found in tumor tissue. The gene encodes a putative transcription factor containing a Cys/His zinc finger domain. The critical homozygous deletions, however, are rarely seen, suggesting that in many cases the gene may be inactivated by more subtle alterations. To facilitate the seareh for smaller deletions and point mutations we have established the genomic organization of the WTl gene and have determined the sequence of all 10 exons and flanking intron DNA. The pattern of alternative splicing in two regions has been characterized in detail. These results will form the basis for future studies of mutant alleles at this locus.},
subject = {Biochemie},
language = {en}
}
@article{WolfKlugHackenbergetal.1992,
author = {Wolf, Markus and Klug, J{\"o}rg and Hackenberg, Reinhard and Gessler, Manfred and Grzeschik, Karl-Heinz and Beato, Miguel and Suske, Guntram},
title = {Human CC10, the homologue of rabbit uteroglobin: genomic cloning, chromosomal localization and expression in endometrial cell lines},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59206},
year = {1992},
abstract = {No abstract available},
subject = {Biochemie},
language = {en}
}
@article{VortkampFranzGessleretal.1992,
author = {Vortkamp, Andrea and Franz, Thomas and Gessler, Manfred and Grzeschik, Karl-Heinz},
title = {Deletion of GLI3 supports the homology of the human Greig cephalopolysyndactyly syndrome (GCPS) and the mouse mutant extra toes (Xt)},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-30166},
year = {1992},
abstract = {No abstract available},
language = {en}
}
@article{VortkampThiasGessleretal.1991,
author = {Vortkamp, A. and Thias, U. and Gessler, Manfred and Rosenkranz, W. and Kroisel, P. M. and Tommerup, N. and Kruger, G. and Gotz, J. and Pelz, L. and Grzeschik, Karl-Heinz},
title = {A somatic cell hybrid panel and DNA probes for physical mapping of human chromosome 7p},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59217},
year = {1991},
abstract = {No abstract available},
subject = {Biochemie},
language = {en}
}
@article{GesslerHameisterHenryetal.1990,
author = {Gessler, Manfred and Hameister, H. and Henry, I. and Junien, C. and Braun, T. and Arnold, H. H.},
title = {The human MyoD1 (MYF3) gene maps on the short arm of chromosome 11 but is not associated with the WAGR locus or the region for the Beckwith-Wiedemann syndrome},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59221},
year = {1990},
abstract = {The human gene encoding the myogenic determination factor myf3 (mouse MyoD1) has been mapped to the short arm of chromosome 11. Analysis of several somatic cell hybrids containing various derivatives with deletions or translocations revealed that the human MyoD (MYF3) gene is not associated with the WAGR locus at chromosomal band 11pl3 nor with the loss of the heterozygosity region at 11p15.5 related to the Beckwith-Wiedemann syndrome. Subregional mapping by in situ hybridization with an myf3 specific probe shows that the gene resides at the chromosomal band llp14, possibly at llp14.3.},
subject = {Biochemie},
language = {en}
}
@article{vanHeyningenBickmoreSeawrightetal.1990,
author = {van Heyningen, V. and Bickmore, W. A. and Seawright, A. and Fletcher, J. M. and Maule, J. and Fekete, G. and Gessler, Manfred and Bruns, G. A. and Huerre-Jeanpierre, C. and Junien, C.},
title = {Role for the Wilms tumor gene in genital development?},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59238},
year = {1990},
abstract = {No abstract available},
subject = {Biochemie},
language = {en}
}
@article{GesslerPoustkaCaveneeetal.1990,
author = {Gessler, Manfred and Poustka, Annemarie and Cavenee, Webster and Neve, Rachael L. and Orkin, Stuart H. and Bruns, Gail A.},
title = {Homozygous deletion in Wilms tumours of a zinc-finger gene identified by chromosome jumping},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-30122},
year = {1990},
abstract = {No abstract available},
language = {en}
}
@article{GesslerBruns1989,
author = {Gessler, Manfred and Bruns, G. A. P.},
title = {A physical map around the WAGR complex on the short arm of chromosome 11},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59246},
year = {1989},
abstract = {A long-range restriction map of part of the short arm of ehromosome 11 including the WAGR region has been constructed using pulsed-field gel electrophoresis and a number of infrequently cutting restriction enzymes. A total of 15.4 Mbp has been mapped in detall, extending from proximal 11p14 to the distal part of 11p12. The map localizes 35 different DNA probes and reveals at least nine areas with features eharaeteristle of BTF islands, some of which may be candidates for the different loci underlying the phenotype of the WAGR syndrome. This map will furthermore allow screening of DNA from individuals with WAGR-related phenotypes and from Wilms tumors for associated chromosomal rearrangements.},
subject = {Biochemie},
language = {en}
}
@article{GesslerThomasCouillinetal.1989,
author = {Gessler, Manfred and Thomas, G. H. and Couillin, P. and Junien, C. and McGillivray, B. C. and Hayden, M. and Jaschek, G. and Bruns, G. A.},
title = {A deletion map of the WAGR region on chromosome II},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59255},
year = {1989},
abstract = {The WAGR (Wilms tumor, aniridia, genitourinary anomalies, and mental retardation) region has been assigned to chromosome 11p13 on the basis of overlapping constitutional deletions found in affected individuals. We have utilized 31 DNA probes which map to the WAGR deletion region, together with six reference loci and 13 WAGR-related deletions, to subdivide this area into 16 intervals. Specific intervals have been correlated with phenotypic features, leading to the identification of individual subregions for the aniridia and Wilms tumor loci. Delineation, by specific probes, of multiple intervals above and below the critical region and of five intervals within the overlap area provides a framework map for molecular characterization of WAGR gene loci and of deletion boundary regions.},
subject = {Biochemie},
language = {en}
}
@article{GesslerBruns1988,
author = {Gessler, Manfred and Bruns, Gail A. P.},
title = {Molecular mapping and cloning of the breakpoints of a chromosome 11p14.1-p13 deletion associated with the AGR syndrome},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59264},
year = {1988},
abstract = {Chromosome 11p13 is frequently rearranged in individuals with the WAGR syndrome (Wilms tumor, aniridia, genitourinary anomalies, and mental retardation) or parts of this syndrome. To map the cytogenetic aberrations molecularly, we screened DNA from cell Unes with known WAGR-related chromosome abnormalities for rearrangements with pulsed fleld gel (PFG) analysis using probes deleted from one chromosome 11 homolog of a WAGR patient. The first alteration was detected in a cell line from an individual with aniridia, genitourinary anomalies, mental retardation, and a deletion described as 11p14.1-p13. We have located one breakpoint close to probe HU11-164B and we have cloned both breakpoint sites as well as the junctional fragment. The breakpoints subdivide current intervals on the genetic map, and the probes for both sides will serve as important additional markers for a long-range restriction map of this region. Further characterization and sequencing of the breakpoints may yield insight into the mechanisms by which these deletions occur.},
subject = {Biochemie},
language = {en}
}
@article{BarnekowGessler1986,
author = {Barnekow, Angelika and Gessler, Manfred},
title = {Activation of the pp60\(^{c-src}\) kinase during differentiation of monomyelocytic cells in vitro},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59278},
year = {1986},
abstract = {Tbe proto-oncogene c-src, the cellular homolog of the Rous sarcoma virus (RSV) transforming gene v-src, is expressed in a tissue-specific and age-dependent manner. Its physiological function, although still unknown, appears to be more closely related to differentiation processes than to proliferation processes. To obtain more information about the physiological role of the c-src gene in cells, we have studied differentiation-dependent alterations using the human HL-60 leukaemia cell line as a model system. Induction of monocytic and granulocytic differentiation of HL-60 cells by 12-0-tetradecanoylphorbol-13-acetate (TPA) and dimethylsulfoxide (DMSO) is associated with an activation of the pp60c-src tyrosine kinase, but not with increased c-src gene expression. Control experiments exclude an interaction of TPA and DMSO themselves with the pp60c-src kinase.},
subject = {Biochemie},
language = {en}
}
@article{GesslerBarnekow1984,
author = {Gessler, Manfred and Barnekow, Angelika},
title = {Differential expression of the cellular oncogenes c-src and c-yes in embryonal and adult chicken tissues},
url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59289},
year = {1984},
abstract = {The cellular onc-genes c-src and c-yes are expressed very differently during chicken embryonic development. The c-src mRNA and its translational product are detectable at high levels in brain extracts of chicken embryos and adult chickens, whereas muscle extracts show an age-dependent decrease in the amounts of c-src-specific mRNA and pp60c-src kinase activity. In contrast, the Ievels of c-yes mRNA in brain, heart, and muscle are relatively low in early embryonic stages and increase later on to values comparable to those found for liver, while in adult animals the pattern of c-yes expression is similar to that of the c-src gene. From the close correlation between the Ievels of pp60c-src, its enzymatic activity, and its corresponding mRNA at a given stage of development and in given tissues, it appears that the expression of pp60c-src is primarily controlled at the level of transcription. It is suggested that because of the different patterns of expression, the two cellular oncogenes, c-src and c-yes, play different roles in cell proliferation during early embryonic stages as weil as in ensuing differentiation processes.},
subject = {Biochemie},
language = {en}
}