Recombinant Human ALDH5A1, His-tagged

• Cat.No.: ALDH5A1-2821H
• Product Overview: Recombinant humanALDH5A1 protein,fused to His-tag at N-terminus, was expressed in E.coli and purified by using conventional chromatography techniques. MW = 54.6 kDa (509aa), confirmed by MALDI-TOF.

Specification

• Cat. No.: ALDH5A1-2821H
• Description: ALDH5A1 belongs to the aldehyde dehydrogenase family of proteins. This protein functions as a mediate the NADP+-dependent oxidation of aldehydes into acids and plays an important role in the detoxification of alcohol-derived acetaldehyde, as well as in lipid peroxidation and in the metabolism of corticosteroids, biogenic amines and neurotransmitters. ALDH5A1 is expressed in a variety of tissues, including liver, heart, lung, brain, kidney and placenta.
• Source: E.coli.
• Sequences Of Amino Acids: MGSSHHHHHH SSGLVPRGSH MAGRLAGLSA ALLRTDSFVG GRWLPAAATF PVQDPASGAA LGMVADCGVR EARAAVRAAY EAFCRWREVS AKERSSLLRK WYNLMIQNKD DLARIITAES GKPLKEAHGE ILYSAFFLEW FSEEARRVYG DIIHTPAKDR RALVLKQPIG VAAVITPWNF PSAMITRKVG AALAAGCTVV VKPAEDTPFS ALALAELASQ AGIPSGVYNV IPCSRKNAKE VGEAICTDPL VSKISFTGST TTGKILLHHA ANSVKRVSME LGGLAPFIVF DSANVDQAVA GAMASKFRNT GQTCVCSNQF LVQRGIHDAF VKAFAEAMKK NLRVGNGFEE GTTQGPLINE KAVEKVEKQV NDAVSKGATV VTGGKRHQLG KNFFEPTLLC NVTQDMLCTH EETFGPLAPV IKFDTEEEAI AIANAADVGL AGYFYSQDPA QIWRVAEQLE VGMVGVNEGL ISSVECPFGG VKQSGLGREG SKYGIDEYLE LKYVCYGGL
• Purity: > 90% by SDS – PAGE.
• Form: Liquid. In 20mM Tris-HCl buffer (pH 8.0) containing 10% glycerol 1mM DTT, 0.1M NaCl, 1mM EDTA.
• Concentration: 0.5 mg/ml (determined by Bradford assay).
• Storage: Can be stored at +4°C short term (1-2 weeks). For long term storage, aliquot and store at -20°C or -70°C. Avoid repeated freezing and thawing cycles.

Gene Information

• Gene Name: ALDH5A1 aldehyde dehydrogenase 5 family, member A1 [ Homo sapiens ]
• Synonyms: ALDH5A1; aldehyde dehydrogenase 5 family, member A1; SSDH; SSADH; succinate-semialdehyde dehydrogenase, mitochondrial; OTTHUMP00000214394; aldehyde dehydrogenase family 5 member A1; mitochondrial succinate semialdehyde dehydrogenase; NAD(+)-dependent succinic semialdehyde dehydrogenase; EC 1.2.1.24
• Gene ID: 7915
• mRNA Refseq: NM_001080
• Protein Refseq: NP_001071
• MIM: 610045
• UniProt ID: P51649
• Chromosome Location: 6p22
• Pathway: Alanine, aspartate and glutamate metabolism; Butanoate metabolism; Metabolic pathways
• Function: oxidoreductase activity; protein homodimerization activity; succinate-semialdehyde dehydrogenase activity

Reviews

10/09/2022

Their expertise and assistance have been invaluable in troubleshooting and providing insightful solutions, greatly enhancing the progress of my experiments.

10/14/2020

The ALDH5A1 Protein's superior stability and functional performance render it an indispensable tool for a wide range of scientific investigations.

08/03/2018

They have proven to be a timely and reliable resource, readily addressing any concerns or challenges that arise during my research.

04/11/2016

What further sets the ALDH5A1 Protein apart is the outstanding technical support provided by the manufacturer.

Q&As

Is ALDH5A1 involved in any other metabolic pathways?

Along with its primary role in GABA metabolism, ALDH5A1 may participate in other metabolic pathways. It has been suggested to be involved in the detoxification of certain aldehydes, although the extent of its contribution to these pathways is not fully understood. Further research is needed to elucidate the involvement of ALDH5A1 in other metabolic processes.

What happens when ALDH5A1 is deficient or mutated?

Deficiency or mutations in ALDH5A1 result in succinic semialdehyde dehydrogenase deficiency (SSADH), also known as GABA-transaminase deficiency. This condition leads to the accumulation of elevated levels of SSA and GABA-related metabolites, impacting GABAergic neurotransmission. SSADH is characterized by various neurological symptoms, including developmental delays, intellectual disability, seizures, ataxia, hypotonia, and behavioral abnormalities.

Are there any known interactions or pathways involving ALDH5A1?

ALDH5A1 is involved in the GABA metabolic pathway, as it plays a crucial role in converting succinic semialdehyde to succinate. It is also implicated in oxidative stress defense mechanisms and has been linked to neurodevelopmental processes, such as neuronal migration and axon guidance.

What are the functions of ALDH5A1 in the body?

ALDH5A1 plays a crucial role in the metabolism of gamma-aminobutyric acid (GABA), a neurotransmitter in the central nervous system. It catalyzes the conversion of succinic semialdehyde (SSA) to succinate, preventing the accumulation of SSA and GABA-related metabolites. Thus, ALDH5A1 acts as an important enzyme in the GABA degradation pathway, maintaining proper GABA levels and neuronal function.

Are there any ongoing studies or therapies targeting ALDH5A1?

Yes, there is ongoing research into the development of small molecules and inhibitors that can modulate ALDH5A1 activity for therapeutic purposes. Targeting ALDH5A1 may offer potential treatments for neurological disorders, cancer, and other conditions related to ALDH5A1 dysregulation.

Are there any known genetic variations or mutations in ALDH5A1?

Yes, mutations in the ALDH5A1 gene are associated with succinic semialdehyde dehydrogenase deficiency (SSADH). These mutations can lead to reduced enzyme activity or protein instability, resulting in the accumulation of toxic levels of succinic semialdehyde and GABA-related metabolites.

How is ALDH5A1 relevant to personalized medicine?

ALDH5A1 activity and expression levels could serve as biomarkers to predict drug response and optimize treatment strategies. Determining an individual's ALDH5A1 status may help personalize medication regimens for better therapeutic outcomes.

Is ALDH5A1 associated with any diseases or disorders?

Yes, mutations or dysregulation in the ALDH5A1 gene can lead to a disorder called succinic semialdehyde dehydrogenase deficiency (SSADH). This condition disrupts GABA metabolism and is associated with various neurological symptoms, such as developmental delay, intellectual disability, and seizures.

Is ALDH5A1 expressed in other tissues besides the brain?

Yes, while ALDH5A1 is primarily expressed in the brain, it is also found in other tissues, albeit at lower levels. ALDH5A1 expression has been reported in the liver, kidney, heart, and other organs, indicating its involvement in other metabolic processes outside the central nervous system.

How is ALDH5A1 regulated?

The expression and activity of ALDH5A1 can be regulated at various levels. Transcriptional regulation through specific transcription factors can control the gene expression of ALDH5A1. Additionally, post-translational modifications, such as phosphorylation or acetylation, can modulate the protein's activity. Various signaling pathways and genetic factors can influence ALDH5A1 regulation.

How is ALDH5A1 deficiency diagnosed?

ALDH5A1 deficiency is typically diagnosed through biochemical tests, such as measuring elevated levels of GABA and SSA in body fluids, including urine and cerebrospinal fluid. Genetic testing is also performed to confirm the presence of mutations in the ALDH5A1 gene. Additionally, clinical evaluation and neurological assessment may be conducted to evaluate the symptoms and presentation of the individual.

Are there any known natural inhibitors or activators of ALDH5A1?

While natural inhibitors or activators specific to ALDH5A1 have not been extensively studied, certain compounds that modulate the activity or expression of aldehyde dehydrogenase enzymes in general may indirectly affect ALDH5A1 as well. For instance, some chemicals or drugs can inhibit or activate aldehyde dehydrogenases, which potentially includes ALDH5A1, depending on their specificity.

Can ALDH5A1 be used as a potential therapeutic target?

Targeting ALDH5A1 holds promise for therapeutic intervention, especially in the context of succinic semialdehyde dehydrogenase deficiency (SSADH). Developing drugs or treatments that can modulate ALDH5A1 activity or stabilize the mutated protein could potentially ameliorate the symptoms associated with this disorder. However, further research is needed to fully understand the implications and feasibility of targeting ALDH5A1 for therapeutic purposes.