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

First Author  Schwartzberg PL Year  1991
Journal  Cell Volume  65
Issue  7 Pages  1165-75
PubMed ID  2065353 Mgi Jnum  J:14644
Mgi Id  MGI:62808 Doi  10.1016/0092-8674(91)90012-n
Citation  Schwartzberg PL, et al. (1991) Mice homozygous for the ablm1 mutation show poor viability and depletion of selected B and T cell populations. Cell 65(7):1165-75
abstractText  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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