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The major pathway for the biosynthesis of phosphatidylcholine occurs via the CDP-choline pathway. Additionally we are shipping Choline Kinase alpha Antibodies (56) and Choline Kinase alpha Proteins (7) and many more products for this protein.
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We found levels of CHKA to be increased in human HCCs (show HCCS ELISA Kits) compared to nontumor tissues, and increased expression to be associated with tumor aggressiveness. Overexpression of CHKA in HCC (show FAM126A ELISA Kits) cell lines increased their invasiveness, resistance to EGFR (show EGFR ELISA Kits) inhibitors, and ability to form metastatic tumors in mice by promoting interaction of EGFR (show EGFR ELISA Kits) with mechanistic target of rapamycin (show FRAP1 ELISA Kits) complex 2.
Study shows increased CHKA expression in pancreatic ductal adenocarcinoma tumors and may be a predictive marker of response to chemotherapy.
These data also support the approach of antitumor strategies that destabilize Chk-alpha protein or downregulate PtdCho in breast cancer treatment.
Downregulation of choline kinase-alpha enhances autophagy in tamoxifen-resistant breast cancer cells.
CHKA can act as an AR chaperone, providing, to our knowledge, the first evidence for kinases as molecular chaperones, making CHKA both a marker of tumor progression and a potential therapeutic target for PCa (show FLVCR1 ELISA Kits).
Identify choline kinase alpha as a key regulator of glutathione-dependent antioxidant cell defense in ovarian carcinoma.
choline kinase alpha is inhibited by a near-infrared fluorescent carbocyanine
Increased expression of CHKA is seen in malignant lesions of prostate cancer
Chokalpha possessed oncogenic activity and could be a potential therapeutic target in T-cell lymphoma , as well as other hematological malignancies with interrupted Ras signaling pathways
Downregulation of Chk-alpha with siRNA increased PLD1 expression, and downregulation of PLD1 increased Chk-alpha expression.
hepatic phosphatidylcholine (show SGMS2 ELISA Kits) is regulated by the circadian clock through a Bmal1 (show ARNTL ELISA Kits)-Rev-erbalpha (show NR1D1 ELISA Kits)-Chkalpha axis
Enforced expression of either CK(alpha) or CCTalpha (show PCYT1A ELISA Kits) increased the rate of synthesis and the amount of PtdCho, and these cells initiated neuronal differentiation.
Lack of muscle degeneration in forelimbs of Chkb (show CHKB ELISA Kits)(-/-) mice is due to abundant choline kinase alpha and the stable homeostasis of phosphatidylcholine (show SGMS2 ELISA Kits).
Experimental evidence for the presence of heteromeric ChoK/EtnK in any source. The activity of ChoK/EtnK in the cell is controlled not only by the level of each isoform but also by their combination to form the active oligomer complex.
ChoK may have a role in carcinogenesis
Data suggest that the choline kinase alpha promoter has a distal element (-875/-867) that binds c-jun (show JUN ELISA Kits) and the binding of c-jun (show JUN ELISA Kits) is enhanced by treatment with CCl4 (show CCL4 ELISA Kits).
Chka is an essential gene for early embryonic development, but adult mice do not require full expression of the gene for normal levels of phosphatidylcholine (show SGMS2 ELISA Kits).
The major pathway for the biosynthesis of phosphatidylcholine occurs via the CDP-choline pathway. The protein encoded by this gene is the initial enzyme in the sequence and may play a regulatory role. The encoded protein also catalyzes the phosphorylation of ethanolamine. Two transcript variants encoding different isoforms have been found for this gene.
choline kinase alpha
, choline kinase beta
, choline kinase
, ethanolamine kinase
, choline/ethanolamine kinase alpha
, choline kinase R