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  • 1990-1994  (7)
  • 1
    Online Resource
    Online Resource
    Mast cell number in the skin of heterozygotes reflects the molecular nature of c-kit mutation
    American Society of Hematology ; 1993
    In:  Blood Vol. 81, No. 10 ( 1993-05-15), p. 2530-2538
    Details
    In: Blood, American Society of Hematology, Vol. 81, No. 10 ( 1993-05-15), p. 2530-2538
    Abstract: The W locus of mice encodes the c-kit receptor tyrosine kinase. Heterozygous WJic/+ and Wn/+ mice and homozygous Wf/Wf mice were similar in appearance; all of them have large depigmented areas lacking any well-defined pattern. The WJic, Wn, and Wf mutant alleles were characterized and their molecular nature was correlated with the mast cell differentiation in the skin and the biologic features of cultured mast cell (CMC). All WJic, Wn, and Wf were point mutations at the tyrosine kinase domain, and c-kit mRNA was normally transcribed from all of them. The mature 145-Kd form of the c-kit protein was produced from the WJic and Wf alleles, but not from the Wn allele. c-kit proteins produced by the WJic or Wf allele were expressed on the surface of CMCs, but those of the Wn allele were not. When double heterozygous mice were produced between W and WJic and between W and Wn, both W/WJic and W/Wn mice lacked skin mast cells. W/WJic CMCs and W/Wn CMCs did not survive in the coculture with fibroblasts. W/WJic CMCs normally attached to fibroblasts, but W/Wn CMCs did not. The defect of W/Wn CMCs in the attachment was attributed to the deficient extracellular expression of the c-kit protein. The number of skin mast cells was compared among WJic/+, Wn/+, Wf/+, and Wf/Wf mice. Mast cells decreased in WJic/+ and Wf/Wf mice, but not in Wn/+ and Wf/+ mice. Although the Wn was a point mutation at the kinase domain, the biologic effect of the Wn was comparable with that of the W mutant allele, which produces truncated c-kit protein without the transmembrane domain. The weak phenotype of Wn/+ mice may be explained by the deficient extracellular expression of c-kit proteins produced by the Wn allele. When WJic/WJic, Wn/Wn, and Wf/Wf CMCs were stimulated by the recombinant c-kit ligand, autophosphorylation activity was observed only in Wf/Wf CMCs. This result was consistent with the weak biologic effect of the Wf mutant allele.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V81.10.2530.bloodjournal81102530
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1993
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Characterization of Ws mutant allele of rats: a 12-base deletion in tyrosine kinase domain of c-kit gene
    American Society of Hematology ; 1991
    In:  Blood Vol. 78, No. 8 ( 1991-10-15), p. 1942-1946
    Details
    In: Blood, American Society of Hematology, Vol. 78, No. 8 ( 1991-10-15), p. 1942-1946
    Abstract: Homozygous mutant rats at the newly found white spotting (Ws) locus were anemic and deficient in mast cells and melanocytes. Because the phenotype of Ws/Ws rats resembled the phenotype of mice possessing a double-gene dose of mutant alleles at the W locus and because the c-kit gene was mapped at the W locus of mice, we characterized the c-kit gene of Ws/Ws rats. The authentic sequence of the rat c-kit cDNA was determined by using a cDNA library prepared from the hippocampus of Sprague-Dawley rats. The c-kit cDNA of Ws/Ws and normal (+/+) control rats was obtained by reverse transcriptase modification of the polymerase chain reaction. When compared with the authentic sequence, a deletion of 12 bases was found in the c-kit cDNA of Ws/Ws rats. This change was shown to be a result of the deletion of the genomic DNA. Four amino acids encoded by the deleted 12 bases (ie, Val-Lys-Gly-Asn) were located at two amino acids downstream from the tyrosine autophosphorylation site in the c-kit kinase and were conserved not only in mouse and human c-kit kinases but also in mouse and human c-fms kinases (ie, receptors of colony-stimulating factor-1). Taken together, the Ws/Ws rat is the first characterized mutant of the c-kit gene in an animal species other than the mouse.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V78.8.1942.1942
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1991
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Mast cell number in the skin of heterozygotes reflects the molecular nature of c-kit mutation
    American Society of Hematology ; 1993
    In:  Blood Vol. 81, No. 10 ( 1993-05-15), p. 2530-2538
    Details
    In: Blood, American Society of Hematology, Vol. 81, No. 10 ( 1993-05-15), p. 2530-2538
    Abstract: The W locus of mice encodes the c-kit receptor tyrosine kinase. Heterozygous WJic/+ and Wn/+ mice and homozygous Wf/Wf mice were similar in appearance; all of them have large depigmented areas lacking any well-defined pattern. The WJic, Wn, and Wf mutant alleles were characterized and their molecular nature was correlated with the mast cell differentiation in the skin and the biologic features of cultured mast cell (CMC). All WJic, Wn, and Wf were point mutations at the tyrosine kinase domain, and c-kit mRNA was normally transcribed from all of them. The mature 145-Kd form of the c-kit protein was produced from the WJic and Wf alleles, but not from the Wn allele. c-kit proteins produced by the WJic or Wf allele were expressed on the surface of CMCs, but those of the Wn allele were not. When double heterozygous mice were produced between W and WJic and between W and Wn, both W/WJic and W/Wn mice lacked skin mast cells. W/WJic CMCs and W/Wn CMCs did not survive in the coculture with fibroblasts. W/WJic CMCs normally attached to fibroblasts, but W/Wn CMCs did not. The defect of W/Wn CMCs in the attachment was attributed to the deficient extracellular expression of the c-kit protein. The number of skin mast cells was compared among WJic/+, Wn/+, Wf/+, and Wf/Wf mice. Mast cells decreased in WJic/+ and Wf/Wf mice, but not in Wn/+ and Wf/+ mice. Although the Wn was a point mutation at the kinase domain, the biologic effect of the Wn was comparable with that of the W mutant allele, which produces truncated c-kit protein without the transmembrane domain. The weak phenotype of Wn/+ mice may be explained by the deficient extracellular expression of c-kit proteins produced by the Wn allele. When WJic/WJic, Wn/Wn, and Wf/Wf CMCs were stimulated by the recombinant c-kit ligand, autophosphorylation activity was observed only in Wf/Wf CMCs. This result was consistent with the weak biologic effect of the Wf mutant allele.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V81.10.2530.2530
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1993
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Characterization of Ws mutant allele of rats: a 12-base deletion in tyrosine kinase domain of c-kit gene
    American Society of Hematology ; 1991
    In:  Blood Vol. 78, No. 8 ( 1991-10-15), p. 1942-1946
    Details
    In: Blood, American Society of Hematology, Vol. 78, No. 8 ( 1991-10-15), p. 1942-1946
    Abstract: Homozygous mutant rats at the newly found white spotting (Ws) locus were anemic and deficient in mast cells and melanocytes. Because the phenotype of Ws/Ws rats resembled the phenotype of mice possessing a double-gene dose of mutant alleles at the W locus and because the c-kit gene was mapped at the W locus of mice, we characterized the c-kit gene of Ws/Ws rats. The authentic sequence of the rat c-kit cDNA was determined by using a cDNA library prepared from the hippocampus of Sprague-Dawley rats. The c-kit cDNA of Ws/Ws and normal (+/+) control rats was obtained by reverse transcriptase modification of the polymerase chain reaction. When compared with the authentic sequence, a deletion of 12 bases was found in the c-kit cDNA of Ws/Ws rats. This change was shown to be a result of the deletion of the genomic DNA. Four amino acids encoded by the deleted 12 bases (ie, Val-Lys-Gly-Asn) were located at two amino acids downstream from the tyrosine autophosphorylation site in the c-kit kinase and were conserved not only in mouse and human c-kit kinases but also in mouse and human c-fms kinases (ie, receptors of colony-stimulating factor-1). Taken together, the Ws/Ws rat is the first characterized mutant of the c-kit gene in an animal species other than the mouse.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V78.8.1942.bloodjournal7881942
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1991
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Identification of mutations in the coding sequence of the proto-oncogene c-kit in a human mast cell leukemia cell line causing ligand-independent activation of c-kit product.
    American Society for Clinical Investigation ; 1993
    In:  Journal of Clinical Investigation Vol. 92, No. 4 ( 1993-10-1), p. 1736-1744
    Details
    In: Journal of Clinical Investigation, American Society for Clinical Investigation, Vol. 92, No. 4 ( 1993-10-1), p. 1736-1744
    Type of Medium: Online Resource
    ISSN: 0021-9738
    URL: Article
    DOI: 10.1172/JCI116761
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 1993
    detail.hit.zdb_id: 2018375-6
    Location Call Number Limitation Availability
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    Online Resource
  • 6
    Online Resource
    Online Resource
    c-kit Gene was not transcribed in cultured mast cells of mast cell- deficient Wsh/Wsh mice that have a normal number of erythrocytes and a normal c-kit coding region
    American Society of Hematology ; 1992
    In:  Blood Vol. 80, No. 6 ( 1992-09-15), p. 1448-1453
    Details
    In: Blood, American Society of Hematology, Vol. 80, No. 6 ( 1992-09-15), p. 1448-1453
    Abstract: The Wsh is a mutant allele at the W (c-kit) locus of mice. Mice of Wsh/Wsh genotype have white hairs and black eyes. Although adult C57BL/6-Wsh/Wsh mice were not anemic, they showed a remarkable depletion of mast cells. Most homozygous or double heterozygous mutant mice at the W (c-kit) locus, of which mast-cell depletion was comparable to that of Wsh/Wsh mice, are deficient in germ cells. However, male and female Wsh/Wsh mice have an appreciable number of germ cells in their gonads. We investigated the mechanism of specific depletion of mast cells in Wsh/Wsh mice. Cultured mast cells (CMC) derived from the spleen of Wsh/Wsh mice neither attached to normal (+/+) fibroblasts nor survived in the coculture with +/+ fibroblasts. The c-kit messenger RNA (mRNA) was strongly expressed in +/+ CMC, but not detectable in Wsh/Wsh CMC. Despite the lack of c-kit mRNA in Wsh/Wsh CMC, the c-kit mRNA was normally detectable in the cerebellum and weakly detectable in the testis and spleen of Wsh/Wsh mice. No significant changes were found in the nucleotide sequence of the c-kit transcripts obtained from the cerebellum of Wsh/Wsh mice. Development of mast cells, erythrocytes, and germ cells in Wsh/Wsh mice appeared to be parallel with the magnitude of the c-kit gene expression in each cell type.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V80.6.1448.1448
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1992
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    c-kit Gene was not transcribed in cultured mast cells of mast cell- deficient Wsh/Wsh mice that have a normal number of erythrocytes and a normal c-kit coding region
    American Society of Hematology ; 1992
    In:  Blood Vol. 80, No. 6 ( 1992-09-15), p. 1448-1453
    Details
    In: Blood, American Society of Hematology, Vol. 80, No. 6 ( 1992-09-15), p. 1448-1453
    Abstract: The Wsh is a mutant allele at the W (c-kit) locus of mice. Mice of Wsh/Wsh genotype have white hairs and black eyes. Although adult C57BL/6-Wsh/Wsh mice were not anemic, they showed a remarkable depletion of mast cells. Most homozygous or double heterozygous mutant mice at the W (c-kit) locus, of which mast-cell depletion was comparable to that of Wsh/Wsh mice, are deficient in germ cells. However, male and female Wsh/Wsh mice have an appreciable number of germ cells in their gonads. We investigated the mechanism of specific depletion of mast cells in Wsh/Wsh mice. Cultured mast cells (CMC) derived from the spleen of Wsh/Wsh mice neither attached to normal (+/+) fibroblasts nor survived in the coculture with +/+ fibroblasts. The c-kit messenger RNA (mRNA) was strongly expressed in +/+ CMC, but not detectable in Wsh/Wsh CMC. Despite the lack of c-kit mRNA in Wsh/Wsh CMC, the c-kit mRNA was normally detectable in the cerebellum and weakly detectable in the testis and spleen of Wsh/Wsh mice. No significant changes were found in the nucleotide sequence of the c-kit transcripts obtained from the cerebellum of Wsh/Wsh mice. Development of mast cells, erythrocytes, and germ cells in Wsh/Wsh mice appeared to be parallel with the magnitude of the c-kit gene expression in each cell type.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V80.6.1448.bloodjournal8061448
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1992
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
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