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anti-Human CPS1 Antikörper:
anti-Rat (Rattus) CPS1 Antikörper:
anti-Mouse (Murine) CPS1 Antikörper:
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Human Monoclonal CPS1 Primary Antibody für IHC (p), ELISA - ABIN560455
Lee, Jee, Kwon, Yoon, Xu, Wang, Wang, Thorgeirsson, Lee, Woo, Yoon: Identification of a mitochondrial defect gene signature reveals NUPR1 as a key regulator of liver cancer progression. in Hepatology (Baltimore, Md.) 2015
Dog (Canine) Polyclonal CPS1 Primary Antibody für IHC, IHC (p) - ABIN4300273
van Straten, van Steenbeek, Grinwis, Favier, Kummeling, van Gils, Fieten, Groot Koerkamp, Holstege, Rothuizen, Spee: Aberrant expression and distribution of enzymes of the urea cycle and other ammonia metabolizing pathways in dogs with congenital portosystemic shunts. in PLoS ONE 2014
CPS1 maintains pyrimidine pools and DNA synthesis in KRAS/LKB1 (zeige STK11 Antikörper)-mutant lung cancer cells
CPS1 knockdown reduced cell growth, decreased levels of metabolites associated with nucleic acid biosynthesis.
These results may offer an increasing understand that CPS1 might have a function in differentiation.
Molecular structure of CPS1 has been deciphered.
CPS1 and CPS1IT1 may be potential prognostic indicators for patients with intrahepatic cholangiocarcinoma.
CPS1 is involved in the urea cycle in weight maintenance.
More HCC (zeige FAM126A Antikörper) cells could be identified by the antibody cocktail for CPS1 and P-CK compared with a single antibody.
characterized the only currently known recurrent CPS1 mutation, p.Val1013del found in eleven unrelated patients of Turkish descent; mutation p.V1013del inactivates CPS1 but does not render the enzyme grossly unstable or insoluble
Overexpression of CPS1 is associated with rectal cancers.
study examined patient characteristics, including genetic polymorphism, to identify risk factors associated with development of hyperammonemia during valproic acid-based therapy; found CPS1 4217C>A polymorphism may not be associated with development of hyperammonemia in Japanese population
these data suggest that AhR (zeige AHR Antikörper) activation promotes CPS1 recruitment to DNA enhancer sites in the genome, resulting in a specific enzyme-independent post-translational modification of the linker histone H1 (zeige H1F0 Antikörper) protein (H1K34hcit), pivotal in altering local chromatin structure and transcriptional activation.
The results suggest that elevated isoaspartate and CPS-1, and reduced CA-III (zeige CA3 Antikörper) levels could serve as biomarkers of hepatocellular injury.
CPS1 becomes readily detectable upon hepatocyte apoptotic and necrotic death. Its abundance and short serum half-life suggest that it may be a useful prognostic biomarker in acute liver injury.
Taken together with previous findings regarding CPS1 structure and function, homology modeling of mouse CPS1 suggested that nitration at Y1450 in an alpha-helix of allosteric domain prevents activation of CPS1 by its activator, N-acetyl-l-glutamate (zeige GRIN1 Antikörper).
Because ammonia generated during fasting is toxic, SIRT5 (zeige SIRT5 Antikörper) protein might play a protective role by converting ammonia to non-toxic urea through deacetylation and activation of CPS1.
Y-box binding protein-1 (zeige YBX1 Antikörper) down-regulates expression of carbamoyl phosphate synthetase-I by suppressing CCAAT enhancer-binding protein-alpha (zeige CEBPA Antikörper) function in mice.
SIRT5 (zeige SIRT5 Antikörper) deacetylates CPS1 and upregulates its activity
The mitochondrial enzyme encoded by this gene catalyzes synthesis of carbamoyl phosphate from ammonia and bicarbonate. This reaction is the first committed step of the urea cycle, which is important in the removal of excess urea from cells. The encoded protein may also represent a core mitochondrial nucleoid protein. Three transcript variants encoding different isoforms have been found for this gene. The shortest isoform may not be localized to the mitochondrion. Mutations in this gene have been associated with carbamoyl phosphate synthetase deficiency, susceptibility to persistent pulmonary hypertension, and susceptibility to venoocclusive disease after bone marrow transplantation.
carbamoyl-phosphate synthase [ammonia], mitochondrial
, carbamoylphosphate synthetase I
, carbamoyl phosphate synthetase 1
, carbamoyl-phosphate synthetase 1, mitochondrial
, carbamyl phosphate synthetase 1
, CPSase I
, carbamoyl-phosphate synthetase I
, carbamyl phosphate synthetase I
, carboamyl-phosphate synthetase 1
, carbamoyl-phosphate synthase 1, mitochondrial
, carbamoyl-phosphate synthase [ammonia], mitochondrial-like
, carbamoyl-phosphate synthetase III
, LOW QUALITY PROTEIN: carbamoyl-phosphate synthase [ammonia], mitochondrial
, carbamoyl-phosphate synthetase 1