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The findings reported herein indicate that palmitate-induced cisternal endoplasmic reticulum expansion is dependent on the activation of XBP-1/CCTalpha-mediated phospholipid accumulation in RAW 264.7 cells.
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Data suggest that CTalpha is an important factor in hepatocyte proliferation in vitro; however, liver regeneration, DNA synthesis, and phosphatidylcholine biosynthesis after partial hepatectomy are not impaired in CTalpha(-/-) knockout mice.
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CaMKI vies with CRM1/exportin 1 for access to a nuclear export signal, and assembly of a CaMKI-14-3-3 zeta-CCTalpha complex is a key effector mechanism that drives nuclear CCTalpha translocation.
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This study illustrates, for the first time, the connection between the acute accumulation of farnesylated prelamin A and involvement of CCT-alpha in generating an nucleoplasmic reticulum.
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Enforced expression of either CK(alpha) or CCTalpha increased the rate of synthesis and the amount of PtdCho, and these cells initiated neuronal differentiation.
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14-3-3zeta controls CCTalpha nuclear import in response to calcium signals, thereby regulating mammalian phospholipid synthesis.
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activation during the S phase of the cell cycle is mediated by the transcription factor Sp1
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cyclin-dependent kinase 2 (CDK2) phosphorylation of Sp1 activates CTalpha transcription during S phase.
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hepatic CTalpha has a role in regulating both hepatic and systemic lipid and lipoprotein metabolism
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ssion of CCTalpha increases surfactant PtdCho synthesis without affecting surfactant protein levels but disrupts glycogen metabolism in differentiating type II cells via its regulatory domain
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a physiologically relevant phosphorylation site and docking domain within CCTalpha serve as targets for ERKs, resulting in inhibition of surfactant synthesis
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CCTalpha expression is required for early embryonic development.
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SCD1 deficiency specifically increases CTP:choline cytidylyltransferase activity by promoting its translocation into membrane and enhances phosphatidylcholine biosynthesis in liver
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CTP:phosphocholine cytidylyltransferase (CT) messenger RNA(mRNA) increased at S-M phase corresponding to an increase of Ets-1 protein mRNA and decrease of Net protein mRNA indicating that Net is an important endogenous repressor for CTalpha transcription
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These observations suggest a role for JNK kinases as negative regulators of phospholipid synthesis in murine lung epithelia.
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HDAC1 plays a critical role in CTalpha repression and that Sp1 and E2F may serve as key targets for HDAC1-mediated CTalpha repression in fibroblasts
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The studies demonstrate that developmental induction of surfactant phospholipid is due, at least in part, to transcriptional activation of the CCTalpha gene.
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CCTalpha was not required for the proliferation or differentiation of lung epithelia but was essential for the secretory component of phospholipid synthesis and critical for the proper formation of lamellar bodies and surfactant protein homeostasis.
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CaM, by antagonizing calpain, serves as a novel binding partner for CCTalpha that stabilizes the enzyme under proinflammatory stress
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When knock-out hepatocytes were infected with an adenovirus expressing CTalpha, apoAI-dependent PC efflux returned partially, whereas cholesterol efflux and ABCA1 levels were not restored to normal levels.
