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Amino Acid Metabolism

All bodily tissues have, to an extent, some ability to synthesize non-essential amino acids, remodel amino acids, and convert carbon skeletons into amino acids and other derivatives that contain nitrogen. All amino acids contain similar structures, including a nitrogen containing amine group. The nitrogen is both an essential part to an amino acid, and also a toxic part of amino acid metabolism. When amino acid intake via diet is plentiful, the metabolism of amino acids via nitrogen metabolism is in full swing. This means there are excess amino acids in circulation, and those that are not used by the body to build its structures are broken down via amino acid metabolism. Entire proteins taken in from diet are initially broken down in the stomach, while the main site of nitrogen or amino acid metabolism is the liver. The deamination of amino acids occurs when the amino group is transferred to other molecules using amino transferase enzymes to form keto acids. These keto acids can be used for energy by the body, converted to glucose, or stored as fat. The end result of deamination releases ammonia and urea. These compounds are then released in the urine.

Anti-PRODH antibody binds against the target proline dehydrogenase (oxidase)1. PRODH is localized on the matrix of the mitochondria and expressed in lung, skeletal muscle, brain, heart, and kidney tissues. Defects in PRODH are the cause of hyperprolinemia type 1 and susceptibility to schizophrenia type 4. People with hyperprolinemia type 1 are often asymptomatic, and thus sometimes go undiagnosed. Affected individuals have increased levels of proline in their blood. When symptoms are seen, they include seizures, mental retardation, and neurological problems. Schizophrenia is a mental disorder characterized by difficulties perceiving reality including auditory hallucinations, delusions, and disorganized speech. Anti-MTHFR antibody binds against the target MTHFR. MTHFR catalyzes the conversion of a co-substrate for homocysteine remethylation to methionine. Defects in MTHFR are the cause of methylenetetrahydrofolate reductase deficiency. Methylenetetrahydrofolate reductase deficiency is a hereditary ocular disease accompanied by symptoms like intellectual disability, psychosis, weakness, ataxia, spasticity, and homocystinuria.

 
Product Number Title Applications Host Clonality
AC16-0031 Anti-Nitrotyrosine Antibody IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)
AC16-0032 Anti-Nitrotyrosine Antibody ELISA, WB, IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (2E11-3D3)
AC16-0046 Anti-Oct4 Antibody WB Rabbit Polyclonal
AC16-0031-01 Anti-Nitrotyrosine Antibody (AMCA) IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)
AC16-0031-02 Anti-Nitrotyrosine Antibody (AP) IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)
AC16-0031-03 Anti-Nitrotyrosine Antibody (APC) IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)
AC16-0031-04 Anti-Nitrotyrosine Antibody (APC-Cy5.5) IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)
AC16-0031-05 Anti-Nitrotyrosine Antibody (APC-Cy7) IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)
AC16-0031-06 Anti-Nitrotyrosine Antibody (Avidin) IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)
AC16-0031-07 Anti-Nitrotyrosine Antibody (Biotin) IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)
AC16-0031-08 Anti-Nitrotyrosine Antibody (BPE) IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)
AC16-0031-09 Anti-Nitrotyrosine Antibody (Cy3) IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (6B2-3G2)