Article Abstract:
In homozygous E2F-5 knockout embryos and mice, embryonic development seemed normal, but newborn mice in time had nonobstructive hydrocephalus. That indicates too much cerebrospinal fluid (CSF). Even though the CSF-producing choroid plexus had normal cell organization it had abundant electron-lucent epithelial cells. That would indicate too much CSF secretion. E2F-5 CNS expression in normal animals was mostly from the choroid plexus. Cell cycle kinetics were not altered in homozygous knockout embryo fibroblasts. E2F-5 is not required for cell proliferation. It changes secretory behavior of differentiated neural tissue.
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Article Abstract:
Suppressor of cytokine signaling-1 (SOCS1), a vital inhibitor of interferon gamma (IFN-gamma) signaling, is discussed. It prevents the potentially fatal neonatal actions of IFN-gamma. The mice exhibit inappropriately intense responses typical of those induced by IFN-gamma and are hyperresponsive to virus infection. They also had macrophages with an enhanced IFN-gamma-dependent capacity to kill L. major parasites. Administering anti-IFN-gamma antibodies prevented the complex disease in the mice.
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Article Abstract:
Deficiency in Suppressor of Cytokine Signaling 1 (SOCS1) has been found to result in accelerated mammary gland development and to rescue lactation in mice lacking prolactin receptors. Mechanisms by which intracellular signaling activated by prolactin is attenuated were not yet defined, so mice with targeted deletions of the SOCS1 and IFN gamma genes were studied.
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