Mice homozygous for the ablm1 mutation show poor viability and depletion of selected B and T cell populations

The c- abl gene, originally identified as the cellular homolog of the transforming gene of the Abelson murine leukemia virus, encodes a protein-tyrosine kinase of unknown function that is expressed in all mammalian tissues. We have previously described the introduction of a mutation in the c- abl ge...

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Published inCell Vol. 65; no. 7; pp. 1165 - 1175
Main Authors Schwartzberg, Pamela L., Stall, Alan M., Hardin, Jeff D., Bowdish, Katherine S., Humaran, Teresa, Boast, Sharon, Harbison, Margaret L., Robertson, Elizabeth J., Goff, Stephen P.
Format Journal Article
LanguageEnglish
Published Cambridge, MA Elsevier Inc 28.06.1991
Cell Press
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Summary:The c- abl gene, originally identified as the cellular homolog of the transforming gene of the Abelson murine leukemia virus, encodes a protein-tyrosine kinase of unknown function that is expressed in all mammalian tissues. We have previously described the introduction of a mutation in the c- abl gene into the mouse germline via targeted gene disruption of embryonic stem cells. We now show that mice homozygous for this mutation are severely affected, displaying increased perinatal mortality, runtedness, and abnormal spleen, head, and eye development. We have examined components of the immune system and have found major reductions in B cell progenitors in the adult bone marrow, with less dramatic reductions in developing T cell compartments.
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ISSN:0092-8674
1097-4172
DOI:10.1016/0092-8674(91)90012-N