HAL
HAL (histidine ammonia-lyase, also known as HIS) is a cytosolic enzyme that catalyses the first reaction in histidine catabolism. It carries out the non-oxidative deamination of L-histidine to trans-urocanic acid. Browse Assay Genie's current range of HAL research reagents below, or read on for the biology behind the target.
HAL catalyses the first step of histidine breakdown. The enzyme removes ammonia from L-histidine in a non-oxidative deamination, producing trans-urocanic acid. Because this is the entry point of the histidine catabolic route, HAL activity determines how histidine is committed to downstream degradation. NCBI Gene describes the enzyme as cytosolic.
The human HAL gene encodes a protein that belongs to the PAL/histidase family. HGNC classifies it within the carbon-nitrogen lyases, consistent with its EC 4.3.1.3 activity. Mouse and rat both carry an orthologous gene named Hal. RefSeq reports that several transcript variants encoding different isoforms have been found for this gene, so researchers working with the HAL protein should consider which isoform is relevant to their question.
HAL is relevant to human disease through histidinemia. According to the NCBI Gene summary, defects in histidine ammonia-lyase cause this condition, which is characterised by increased histidine and histamine and decreased urocanic acid in body fluids. This makes HAL a useful reference point for studies of amino acid catabolism and of the metabolic consequences of its loss. The gene symbol HAL has the previous alias HIS, which may appear in older literature.
HAL catalyses the first reaction in histidine catabolism, making it a central enzyme for studying how L-histidine is broken down.
Defects in HAL cause histidinemia, so the enzyme is a key target for work on this inherited metabolic condition.
HAL produces trans-urocanic acid from L-histidine, and reduced urocanic acid is seen in body fluids when the enzyme is defective.
As a member of the PAL/histidase family of carbon-nitrogen lyases, HAL is a model for non-oxidative deamination chemistry.
HAL, or histidine ammonia-lyase, catalyses the first reaction in histidine catabolism. It performs the non-oxidative deamination of L-histidine to trans-urocanic acid. NCBI Gene describes it as a cytosolic enzyme, and it is classed as a carbon-nitrogen lyase (EC 4.3.1.3).
The gene has the alias HIS, and the protein is named histidine ammonia-lyase. RefSeq reports several transcript variants that encode different isoforms. Check the datasheet of any product for its validated reactivity and the isoforms it is expected to recognise.
Defects in HAL cause histidinemia, marked by increased histidine and histamine and decreased urocanic acid in body fluids. The gene has orthologues in mouse and rat, both named Hal, and the protein belongs to the PAL/histidase family.
Other metabolic enzymes and amino acid catabolism targets with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P42357; product specifications from Assay Genie datasheets.