2.7.7.14: ethanolamine-phosphate cytidylyltransferase
This is an abbreviated version!
For detailed information about ethanolamine-phosphate cytidylyltransferase, go to the full flat file.
Word Map on EC 2.7.7.14
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2.7.7.14
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phosphatidylethanolamine
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phospholipid
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cdp-ethanolamine
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diacylglycerols
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kennedy
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cdp-choline
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ctp:phosphocholine
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phosphocholine
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3hethanolamine
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ptdetn
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ethanolaminephosphotransferase
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14cethanolamine
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drug development
- 2.7.7.14
- phosphatidylethanolamine
- phospholipid
- cdp-ethanolamine
- diacylglycerols
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kennedy
- cdp-choline
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ctp:phosphocholine
- phosphocholine
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3hethanolamine
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ptdetn
- ethanolaminephosphotransferase
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14cethanolamine
- drug development
Reaction
Synonyms
CTP-phosphoethanolamine cytidylyltransferase, CTP:ethanolaminephosphate cytidylyltransferase, CTP:phosphoethanolamine CT, CTP:phosphoethanolamine cytidylyltransferase, CTP:phosphoethanolamine cytidylyltransferase gene, cytidylyltransferase, ethanolamine phosphate, ECT, ET, ethanolamine phosphate cytidylyltransferase, ethanolamine-phosphate cytidylyltransferase, Pcyt2, Pcyt2alpha, Pcyt2beta, PECT1, phosphoethanolamine cytidyltransferase, phosphoethanolamine cytidylyltransferase, phosphorylethanolamine transferase, Tb11.01.5730
ECTree
2.7.7.14 ethanolamine-phosphate cytidylyltransferaseAdvanced search results
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results (Expression
Expression on EC 2.7.7.14 - ethanolamine-phosphate cytidylyltransferase
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EXPRESSION 
ORGANISM
UNIPROT
LITERATURE
25-hydroxycholesterol, an endogenous activator of liver X receptor, and the liver X receptor synthetic agonist TO901317 both significantly reduce the biosynthesis of phosphatidylethanolamine via the CDP-ethanolamine Kennedy pathway by inhibiting the promoter function and expression of Pcyt2 in human MCF-7 cells. The enzyme is downregulated in insulin-resistant muscle
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increased Pcyt2 mRNA levels after serum starvation
increased Pcyt2 mRNA levels after serum starvation are suppressed by 25-hydroxycholesterol. The suppressive effect of 25-hydroxycholesterol on mRNA transcription is ameliorated by trichostatin A. Anacardic acid, 25-hydroxycholesterol and 24(S)-hydroxycholesterol suppress the transcription by inhibiting H3K27 acetylation in the promoter. 27-Hydroxycholesterol, 22(S)-hydroxycholesterol and 22(R)-hydroxycholesterol suppress the transcription
increases after serum starvation
induction of the enzyme by phorbol-12-myristate-13-acetate in hepatocytes. Liver X receptor, LXR, can modulate and activate promoter activity and transcription of Pcyt2. The enzyme is upregulated in obesity-resistant rats and by thiamine supplementation
liver X receptor, LXR, can modulate and activate promoter activity and transcription of Pcyt2. Pcyt2 is transcriptionally up-regulated by serum-deficiency induced differentiation of the skeletal muscle cells C2C12. The core mouse promoter (-111/+29)is dependent on binding of cEBP to an inverse CCAT box located at the position -82/-77 bp, ncreased amount of muscle-specific regulator, MyoD, reduced the content of Sp1 (binds to region -508/-378 bp), which, together with the decrease in ratio of Sp1 to Sp3, is responsible for the stimulation of transcription of Pcyt2 gene in differentiated C2C12 myotubes relative to undifferentiated myoblasts. The enzyme is upregulated in Sirtuin null mice and in adipose tissue of high-weight gainers
liver X receptor, LXR, can modulate and activate promoter activity and transcription of Pcyt2. Pcyt2 is upregulated in methotrexate-resistant HT-29 cells in comparison to a methotrexate-sensitive colon cancer cell line
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oxysterols, 24-hydroxycholesterol, 25-hydroxycholesterol, 27-hydroxycholesterol, and 24(S),25-epoxycholesterol, and mevalonolactate are partially responsible for the inhibition of Pcyt2 transcription. 25-Hydroxycholesterol, an endogenous activator of liver X receptor, and the liver X receptor synthetic agonist TO901317 both significantly reduce the biosynthesis of phosphatidylethanolamine via the CDP-ethanolamine Kennedy pathway by inhibiting the promoter function and expression of Pcyt2 in mouse embryonic fibroblasts. The enzyme is downregulated in sphingosine 1-phosphate lyase null mice and in livers of copper-transporting ATPase ATP7B null mice, downregulation in ATF2 null mice
the important element for transcriptional control of Pcyt2 by 25-HC resides between -56 and -36 in NIH 3T3 cells. Nuclear factor-Y binds at C(-37)CAAT(-41) and Yin Yang1 binds at C(-42)AT(-40) in the Pcyt2 promoter. Nuclear factor-Y is involved in the inhibitory effects of 25-hydroxycholesterol on Pcyt2 transcription
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increased Pcyt2 mRNA levels after serum starvation are suppressed by 25-hydroxycholesterol. The suppressive effect of 25-hydroxycholesterol on mRNA transcription is ameliorated by trichostatin A. Anacardic acid, 25-hydroxycholesterol and 24(S)-hydroxycholesterol suppress the transcription by inhibiting H3K27 acetylation in the promoter. 27-Hydroxycholesterol, 22(S)-hydroxycholesterol and 22(R)-hydroxycholesterol suppress the transcription
increased Pcyt2 mRNA levels after serum starvation are suppressed by 25-hydroxycholesterol. The suppressive effect of 25-hydroxycholesterol on mRNA transcription is ameliorated by trichostatin A. Anacardic acid, 25-hydroxycholesterol and 24(S)-hydroxycholesterol suppress the transcription by inhibiting H3K27 acetylation in the promoter. 27-Hydroxycholesterol, 22(S)-hydroxycholesterol and 22(R)-hydroxycholesterol suppress the transcription
induction of the enzyme by phorbol-12-myristate-13-acetate in hepatocytes. Liver X receptor, LXR, can modulate and activate promoter activity and transcription of Pcyt2. The enzyme is upregulated in obesity-resistant rats and by thiamine supplementation
-
induction of the enzyme by phorbol-12-myristate-13-acetate in hepatocytes. Liver X receptor, LXR, can modulate and activate promoter activity and transcription of Pcyt2. The enzyme is upregulated in obesity-resistant rats and by thiamine supplementation
-
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liver X receptor, LXR, can modulate and activate promoter activity and transcription of Pcyt2. Pcyt2 is transcriptionally up-regulated by serum-deficiency induced differentiation of the skeletal muscle cells C2C12. The core mouse promoter (-111/+29)is dependent on binding of cEBP to an inverse CCAT box located at the position -82/-77 bp, ncreased amount of muscle-specific regulator, MyoD, reduced the content of Sp1 (binds to region -508/-378 bp), which, together with the decrease in ratio of Sp1 to Sp3, is responsible for the stimulation of transcription of Pcyt2 gene in differentiated C2C12 myotubes relative to undifferentiated myoblasts. The enzyme is upregulated in Sirtuin null mice and in adipose tissue of high-weight gainers
-
liver X receptor, LXR, can modulate and activate promoter activity and transcription of Pcyt2. Pcyt2 is transcriptionally up-regulated by serum-deficiency induced differentiation of the skeletal muscle cells C2C12. The core mouse promoter (-111/+29)is dependent on binding of cEBP to an inverse CCAT box located at the position -82/-77 bp, ncreased amount of muscle-specific regulator, MyoD, reduced the content of Sp1 (binds to region -508/-378 bp), which, together with the decrease in ratio of Sp1 to Sp3, is responsible for the stimulation of transcription of Pcyt2 gene in differentiated C2C12 myotubes relative to undifferentiated myoblasts. The enzyme is upregulated in Sirtuin null mice and in adipose tissue of high-weight gainers
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oxysterols, 24-hydroxycholesterol, 25-hydroxycholesterol, 27-hydroxycholesterol, and 24(S),25-epoxycholesterol, and mevalonolactate are partially responsible for the inhibition of Pcyt2 transcription. 25-Hydroxycholesterol, an endogenous activator of liver X receptor, and the liver X receptor synthetic agonist TO901317 both significantly reduce the biosynthesis of phosphatidylethanolamine via the CDP-ethanolamine Kennedy pathway by inhibiting the promoter function and expression of Pcyt2 in mouse embryonic fibroblasts. The enzyme is downregulated in sphingosine 1-phosphate lyase null mice and in livers of copper-transporting ATPase ATP7B null mice, downregulation in ATF2 null mice
-
oxysterols, 24-hydroxycholesterol, 25-hydroxycholesterol, 27-hydroxycholesterol, and 24(S),25-epoxycholesterol, and mevalonolactate are partially responsible for the inhibition of Pcyt2 transcription. 25-Hydroxycholesterol, an endogenous activator of liver X receptor, and the liver X receptor synthetic agonist TO901317 both significantly reduce the biosynthesis of phosphatidylethanolamine via the CDP-ethanolamine Kennedy pathway by inhibiting the promoter function and expression of Pcyt2 in mouse embryonic fibroblasts. The enzyme is downregulated in sphingosine 1-phosphate lyase null mice and in livers of copper-transporting ATPase ATP7B null mice, downregulation in ATF2 null mice
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