1999
DOI: 10.1042/bj3450139
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Intrinsic alcohol dehydrogenase and hydroxysteroid dehydrogenase activities of human mitochondrial short-chain L-3-hydroxyacyl-CoA dehydrogenase

Abstract: The alcohol dehydrogenase (ADH) activity of human shortchain -3-hydroxyacyl-CoA dehydrogenase (SCHAD) has been characterized kinetically. The k cat of the purified enzyme was estimated to be 2.2 min −" , with apparent K m values of 280 mM and 22µM for 2-propanol and NAD + , respectively. The k cat of the ADH activity was three orders of magnitude less than the -3-hydroxyacyl-CoA dehydrogenase activity but was comparable with that of the enzyme's hydroxysteroid dehydrogenase (HSD) activity for oxidizing 17β-o… Show more

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Cited by 29 publications
(31 citation statements)
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“…The biological relevance of some of these Fig. 1 The beta-oxidation of 2-methylbutyryl-CoA in the breakdown of isoleucine and possible other sources of C2-methylated short acyl-CoA compounds enzymatic activities has not been sufficiently proven; the alcohol dehydrogenase activity of HSD10 is marginal (He et al 2000). There is mounting evidence that HSD10 plays a role in the pathogenesis of several adult-onset neurodegenerative disorders, in particular, that through interaction with amyloid β HSD10 mediates mitochondrial toxicity in Alzheimer's disease (Lustbader et al 2004;Tieu et al 2004;Yan et al 1997;Yang et al 2011).…”
Section: Hsd10 and The Hsd17b10 Genementioning
confidence: 99%
“…The biological relevance of some of these Fig. 1 The beta-oxidation of 2-methylbutyryl-CoA in the breakdown of isoleucine and possible other sources of C2-methylated short acyl-CoA compounds enzymatic activities has not been sufficiently proven; the alcohol dehydrogenase activity of HSD10 is marginal (He et al 2000). There is mounting evidence that HSD10 plays a role in the pathogenesis of several adult-onset neurodegenerative disorders, in particular, that through interaction with amyloid β HSD10 mediates mitochondrial toxicity in Alzheimer's disease (Lustbader et al 2004;Tieu et al 2004;Yan et al 1997;Yang et al 2011).…”
Section: Hsd10 and The Hsd17b10 Genementioning
confidence: 99%
“…The erroneous localization of this protein to the endoplasmic reticulum [22] resulted in the designation of SCHAD as endoplasmic reticulum-associated amyloid-b-binding protein. However, it has been proven that SCHAD is localized in the mitochondrial matrix [1,[23][24][25][26][27][28][29]. This finding prompted a report that SCHAD and amyloid-b peptide are both responsible for the mitochondrial toxicity seen in AD [70].…”
Section: Relevance Of Schad To Mental Retardationmentioning
confidence: 99%
“…SCHAD is also known as type 10 17b-hydroxysteroid dehydrogenase (HSD10) [19,[23][24][25][26]. This human mitochondrial multifunctional enzyme [23][24][25][26][27][28] is a potential target for intervention of Alzheimer's disease (AD), Parkinson's disease (PD), infantile neurodegeneration, and other neural disorders [29][30][31][32]. The characteristics of HAD and SCHAD and their impact on human health and disease are further discussed in the following sections.…”
Section: Introductionmentioning
confidence: 99%
“…9 In vitro, SDR5C1 also acts on other substrates, including branched short-chain fatty acids, hydroxysteroids, and sex hormones. [3][4][5][6]10,11 SDR5C1 deficiency causes a mitochondrial disorder known as 'HSD10 disease'. 7 Biochemical diagnosis of HSD10 disease has traditionally relied upon the detection of elevated metabolites from isoleucine breakdown, 12 which are the same metabolites elevated in patients with a-ketothiolase (AKT) deficiency.…”
Section: Introductionmentioning
confidence: 99%