Mice lacking p27(super Kip1) display increased body size, multiple organ hyperplasia, retinal dysplasia, and pituitary tumors
Article Abstract:
Mice lacking the cyclin-dependent kinase (CDK) inhibitor p27(super Kip1) have a large body size, organ hyperplasia and spontaneous pituitary tumors. CDK2 activity increases ten folds in thymocytes lacking p27. The male mice are fertile while females are sterile due to improper ovarian development. The cellular layer pattern development is disrupted in the retinas. However, the lack of the protein has no effect on the inhibitory effect of transforming growth factor beta on the cell cycle or arrest of embryonic fibroblasts in the G1 phase.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1996
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Enhanced growth of mice lacking the cyclin-dependent kinase inhibitor function of p27(super Kip1)
Article Abstract:
The loss of the cyclin-dependent kinase-inhibitory activity of the p27 protein increases growth and produces nodular hyperplasia in the pituitary's intermediate lobe in mice. However, there is no increase in the amount of growth hormone or insulin-like growth factor I. Mutant female mice are sterile due to defective luteal cell-differentiation and disordered estrus cycle. The defects in the hypothalamic-pituitary-ovarian axis change cell proliferation and cause specific endocrine dysfunction.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1996
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Deletion of SHIP or SHP-1 reveals two distinct pathways for inhibitory signaling
Article Abstract:
An inositol polyphosphate 5'-phosphatase, SHIP, and a tyrosine phosphatase, SHP-1, play a key role in the modulation of immune receptor activation by inhibitory coreceptors. A study was conducted to examine the necessity, interaction or redundancy of these signaling molecules. The findings indicate that SHP-1-mediated inhibitory signaling prevents apoptosis while SHIP recruitment attenuates a proapoptotic signal initiated by FcgammaRIIB.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1997
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