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Controls phosphatidylcholine synthesis.. Additionally we are shipping Phosphate Cytidylyltransferase 1, Choline, alpha Antibodies (67) and Phosphate Cytidylyltransferase 1, Choline, alpha Kits (1) and many more products for this protein.
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There is no correlation between single PCYT1A rs712012 and PCYT1A rs7639752 polymorphisms and the incidence of intrauterine fetal death.
PCYT1A mutations were identified in patients with isolated retinal dystrophy (show MERTK Proteins) without any skeletal involvement from two Italian families.
CCT contributes to phospholipid compositional homeostasis. [Review]
PCYT1A-generated phosphatidylcholine (show SGMS2 Proteins) has a role in the normal function of white adipose tissue and insulin (show INS Proteins) action
We report loss-of-function mutations in PCYT1A as the cause of spondylometaphyseal dysplasia with cone-rod dystrophy.
Mutations in PCYT1A cause spondylometaphyseal dysplasia with cone-rod dystrophy
N-Methylaspartate induced nitric oxide synthase activation and nuclear factor-kB subunit p65 (show GORASP1 Proteins) nuclear translocation in A549 cells were responsible for decreased CTP:phosphocholine cytidylyltransferase A expression
Analyses showed genotype effects of PCYT1A genes on spina bifida risk, but did not show evidence of gene-nutrient. interactions.
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.
Data suggest that CTalpha is an important factor in hepatocyte proliferation in vitro; however, liver regeneration, DNA synthesis, and phosphatidylcholine (show SGMS2 Proteins) biosynthesis after partial hepatectomy are not impaired in CTalpha(-/-) knockout mice.
CaMKI (show CAMK1 Proteins) vies with CRM1/exportin 1 (show XPO1 Proteins) for access to a nuclear export signal, and assembly of a CaMKI (show CAMK1 Proteins)-14-3-3 zeta (show YWHAZ Proteins)-CCTalpha complex is a key effector mechanism that drives nuclear CCTalpha translocation.
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.
Enforced expression of either CK(alpha) or CCTalpha increased the rate of synthesis and the amount of PtdCho, and these cells initiated neuronal differentiation.
14-3-3zeta controls CCTalpha nuclear import in response to calcium signals, thereby regulating mammalian phospholipid synthesis.
activation during the S phase of the cell cycle is mediated by the transcription factor Sp1 (show SP1 Proteins)
cyclin-dependent kinase 2 (CDK2 (show CDK2 Proteins)) phosphorylation of Sp1 (show SP1 Proteins) activates CTalpha transcription during S phase.
hepatic CTalpha has a role in regulating both hepatic and systemic lipid and lipoprotein metabolism
ssion of CCTalpha increases surfactant PtdCho synthesis without affecting surfactant protein levels but disrupts glycogen (show GYS1 Proteins) metabolism in differentiating type II cells via its regulatory domain
Controls phosphatidylcholine synthesis.
phosphate cytidylyltransferase 1, choline, alpha
, choline-phosphate cytidylyltransferase A-like
, CCT A
, CT A
, CTP:phosphocholine cytidylyltransferase A
, choline-phosphate cytidylyltransferase A
, phosphorylcholine transferase A
, CTP:phosphocholine cytidylyl transferase
, CTP:phosphocholine cytidylyltransferase alpha
, choline phosphate cytidylyltransferase 1 alpha
, phosphate cytidylyltransferase 1, choline, alpha isoform
, CTP phosphocholine cytidylyl transferase
, Phosphorylcholine transferase A