Isolation and characterization of a zinc finger polypeptide gene at the human chromosome 11 Wilms' tumor locus

  title={Isolation and characterization of a zinc finger polypeptide gene at the human chromosome 11 Wilms' tumor locus},
  author={Katherine M. Call and Tom Glaser and Caryn Y. Ito and Alan Buckler and Jerry Pelletier and Daniel A. Haber and Elise A. Rose and Astrid M. Kral and Herman Yeger and William H. Lewis and Carol Jones and David E. Housman},

Isolation and Characterization of a Novel Zinc-finger Protein with Transcriptional Repressor Activity (*)

Fusion of the upstream regulatory region of ZNF174 to the DNA-binding domain of GAL4 revealed that the gene could confer a repression function on the heterologous DNA- binding domain, and was found to be a novel transcriptional repressor.

Molecular Cloning of the cDNA and Chromosome Localization of the Gene for Human Ubiquitin-conjugating Enzyme 9*

It is concluded that hUBC9 retains striking structural and functional conservation with yUBC 9 and suggest a possible link of the ubiquitin/proteosome proteolytic pathway and the WT1 transcriptional repressor system.

cDNA isolation, genomic structure, regulation, and chromosomal localization of human lung Kruppel-like factor.

The isolation and chromosomal mapping of human LKLF will make it possible to initiate studies devoted to assess the involvement of this gene in human disease(s), and of particular interest is the finding that while sequences in the proximal promoter have diverged between mouse and human, a region of 75 nucleotides is essentially identical.

A novel X-linked member of the human zinc finger protein gene family: isolation, mapping, and expression

Sequence analysis showed that ZNF81 may encode a polypeptide(s) containing tandem arrays of 12 canonical C2H2 zinc fingers of the Krüppel-type at the C-terminus, which supports the hypothesis that it is an expressed, functional member of this multigene family.



Deletions of a DNA sequence in retinoblastomas and mesenchymal tumors: organization of the sequence and its encoded protein.

It is reported that this segment of cDNA is additionally the target of somatic mutations in mesenchymal tumors among patients having no apparent predisposition to retinoblastoma and no previous evidence of retinOBlastoma.

Molecular analysis of chromosome 11 deletions in aniridia-Wilms tumor syndrome.

Analysis of DNA from the cell lines and hybrids and with a cloned cDNA probe has shown that the catalase gene is deleted in four of five patients, and it is concluded these genes are likely to be outside the region 11p12-11p15.

Molecular cloning, sequencing, and mapping of EGR2, a human early growth response gene encoding a protein with "zinc-binding finger" structure.

Early growth response gene-1 (Egr-1) is a mouse gene displaying fos-like induction kinetics in diverse cell types following mitogenic stimulation. Egr-1 encodes a protein with "zinc-binding finger"

A fine-structure deletion map of human chromosome 11p: Analysis of J1 series hybrids

The deletion map provides a basis to position hereditary disease loci on 11p, to distinguish the pattern of recessive mutations in different forms of cancer and, since many of these genes have been mapped in other mammalian species, to study the evolution of a conserved syntenic group.

Human retinoblastoma susceptibility gene: cloning, identification, and sequence

A gene encoding a messenger RNA (mRNA) of 4.6 kilobases, located in the proximity of esterase D, was identified as the retinoblastoma susceptibility (RB) gene on the basis of chromosomal location, homozygous deletion, and tumor-specific alterations in expression.

The retinoblastoma susceptibility gene encodes a nuclear phosphoprotein associated with DNA binding activity

Biochemical fractionation and immunofluorescence studies demonstrate that the majority of the RB protein is located within the nucleus, suggesting that the RB gene product may function in regulating other genes within the cell.

Introduction of a normal human chromosome 11 into a Wilms' tumor cell line controls its tumorigenic expression.

Support is provided for the existence of genetic information on chromosome 11 which can control the malignant expression of Wilms' tumor cells.