Contribution of lipid second messengers to the regulation of phosphatidylcholine synthesis during cell cycle re-entry

Ng, Michael; Kitos, Theresa E.; Cornell, Rosemary B.

doi:10.1016/j.bbalip.2004.09.001

Cited by 26 publications

(27 citation statements)

References 58 publications

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“…At the end of this 30-min pulse, the medium was removed, and cells were washed twice with PBS, and fresh unlabeled DMEM containing 1 mg/ml BSA was added. The [ 3 H]choline uptake was quenched with methanol/water (5:4); the cells were harvested at intervals thereafter, and [ 3 H]PC was measured as described (41). To assess the relative expression levels of the various transfected CCTs for this experiment, parallel dishes with the same cell seeding density and transfection treatment were harvested, and lysates were prepared for Western blot.…”

Section: Molecular Biology and Biochemical Methodsmentioning

confidence: 99%

A 22-mer Segment in the Structurally Pliable Regulatory Domain of Metazoan CTP: Phosphocholine Cytidylyltransferase Facilitates Both Silencing and Activating Functions

Ding

Taneva

Huang

et al. 2012

Journal of Biological Chemistry

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Background:The mechanism whereby CCT is auto-inhibited by its membrane-induced amphipathic helix (m-AH) is unknown. Results: m-AH regions sharing an amphipathic 22-mer element can be interchanged between CCTs with retention of catalytic silencing and activation by lipids. Conclusion:The 22-mer element is the principal auto-inhibitory motif. Significance: Multi-tasking and conformationally malleable motifs are widely used to regulate protein function; the CCT m-AH is a novel example of this.

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Section: Molecular Biology and Biochemical Methodsmentioning

confidence: 99%

A 22-mer Segment in the Structurally Pliable Regulatory Domain of Metazoan CTP: Phosphocholine Cytidylyltransferase Facilitates Both Silencing and Activating Functions

Ding

Taneva

Huang

et al. 2012

Journal of Biological Chemistry

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“…D609 antioxidant/GSH mimetic properties are based on Aß induced oxidative stress [10], effects on cystine/ glutamate antiporter are based on glutamate toxicity in immature hippocampal neurons (do not express glutamate receptors) [16], increase in metabolic activity in 264.7 macrophages is based on MTT assay. D609 inhibited PC synthesis and may directly affect membrane translocation of cytidine triphosphate (CTP): phosphocholine cytidylyltransferase (CCT), the rate-limiting enzyme in PC synthesis [77] or CDP-choline:DAG phosphocholine transferase (CPT), the final step in the PC synthesis [78]. D609 prevented 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced increase in DAG, activation of nuclear CCT activity, and increase in nuclear PC synthesis [79].…”

Section: Discussionmentioning

confidence: 99%

Protection by D609 Through Cell-Cycle Regulation After Stroke

Adibhatla

Hatcher

2010

Mol Neurobiol

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Expressions of cell-cycle regulating proteins are altered after stroke. Cell-cycle inhibition has shown dramatic reduction in infarction after stroke. Ceramide can induce cell-cycle arrest by up-regulation of cyclin-dependent kinase (Cdk) inhibitors p21 and p27 through activation of protein phosphatase 2A (PP2A). Tricyclodecan-9-yl-xanthogenate (D609)-increased ceramide levels after transient middle cerebral artery occlusion (tMCAO) in spontaneously hypertensive rat (SHR) probably by inhibiting sphingomyelin synthase (SMS). D609 significantly reduced cerebral infarction and up-regulated Cdk inhibitor p21 and down-regulated phospho-retinoblastoma (pRb) expression after tMCAO in rat. Others have suggested bFGF-induced astrocyte proliferation is attenuated by D609 due to an increase in ceramide by SMS inhibition. D609 also reduced the formation of oxidized phosphatidylcholine (OxPC) protein adducts. D609 may attenuate generation of reactive oxygen species and formation of OxPC by inhibiting microglia/macrophage proliferation after tMCAO (please also see note added in proof: D609 may prevent mature neurons from entering the cell cycle at the early reperfusion, however may not interfere with later proliferation of microglia/ macrophages that are the source of brain derived neurotrophic factor (BDNF) and insulin-like growth factor (IGF-1) in offering protection). It has been proposed that D609 provides benefit after tMCAO by attenuating hypoxia-inducible factor-1alpha and Bcl2/adenovirus E1B 19 kDa interacting protein 3 expressions. Our data suggest that D609 provides benefit after stoke through inhibition of SMS, increased ceramide levels, and induction of cell-cycle arrest by up-regulating p21 and causing hypophosphorylation of Rb (through increased protein phosphatase activity and/or Cdk inhibition).

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“…The partial G 1 arrest caused by CCT␣ silencing in detached ras4 cells is also consistent with inhibition of PC synthesis. CCT␣ is activated in early G 1 by phospholipid degradation products and contributes to net PC synthesis during S phase (25,29,56). Cessation of PC synthesis in CHO cells expressing temperature-sensitive CCT␣ resulted in G 1 arrest prior to induction of apoptosis (27).…”

Section: Discussionmentioning

confidence: 99%

ras-induced Up-regulation of CTP:Phosphocholine Cytidylyltransferase α Contributes to Malignant Transformation of Intestinal Epithelial Cells

Arsenault

Rosen

Ridgway

2013

Journal of Biological Chemistry

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Background: PC synthesis by the CDP-choline pathway is regulated by CCT␣. Results: Increased expression of nuclear CCT␣ in ras-transformed intestinal epithelial contributes to PC synthesis that is required for anchorage-independent growth. Conclusion: An expanded pool of nuclear CCT␣ is involved in malignant transformation by ras. Significance: CCT␣ is a potential target to restore anchorage-dependent growth sensitivity of cancer cells.

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Contribution of lipid second messengers to the regulation of phosphatidylcholine synthesis during cell cycle re-entry

Cited by 26 publications

References 58 publications

A 22-mer Segment in the Structurally Pliable Regulatory Domain of Metazoan CTP: Phosphocholine Cytidylyltransferase Facilitates Both Silencing and Activating Functions

A 22-mer Segment in the Structurally Pliable Regulatory Domain of Metazoan CTP: Phosphocholine Cytidylyltransferase Facilitates Both Silencing and Activating Functions

Protection by D609 Through Cell-Cycle Regulation After Stroke

ras-induced Up-regulation of CTP:Phosphocholine Cytidylyltransferase α Contributes to Malignant Transformation of Intestinal Epithelial Cells

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