High impact information on Acot2

• The nomenclature for these genes has tentatively been assigned as CTE-I (cytosolic), MTE-I (mitochondrial), and PTE-Ia and Ib (peroxisomal), based on the identification of putative targeting signals [1].
• ACTH and LH regulate the activity of PTPs and Acot2 and promote the induction of ACS4 [2].
• Two of such events are the protein tyrosine dephosphorylation mediated by protein tyrosine phosphatases (PTPs) and the release of arachidonic acid (AA) mediated by two enzymes, ACS4 (acyl-CoA synthetase 4) and Acot2 (mitochondrial thioesterase) [2].
• The constitutive expression of both mRNAs was low in liver, with CTE-I expressed mainly in kidney and brown adipose tissue, and MTE-I expressed in brown adipose tissue and heart [3].
• The promoter regions of both the CTE-I and MTE-I genes contain putative PP response elements, suggesting an involvement of PP-activated receptors in the regulation of these genes [3].

Biological context of Acot2

• To elucidate the role of these enzymes in lipid metabolism, the authors have cloned the cDNAs corresponding to the inducible cytosolic and mitochondrial type I enzymes (CTE-I and MTE-I), and studied tissue expression and nutritional regulation of expression of the mRNAs in mice [3].

Anatomical context of Acot2

• The promoter regions of both the CTE-I and MTE-I genes contain putative peroxisome proliferator response elements (PPREs), suggesting an involvement of peroxisome proliferator-activated receptors in the regulation of these genes [4].
• Reduction in the expression of the mitochondrial acyl-CoA thioesterase (MTE-I) by antisense or small interfering RNA (siRNA) and of the arachidonic acid-preferring acyl-CoA synthetase (ACS4) by siRNA produced a marked reduction in steroid output of cAMP-stimulated Leydig cells [5].

Associations of Acot2 with chemical compounds

• As expected, the expression in liver of both the CTE-I and MTE-I mRNAs were strongly induced (> 50-fold) by treatment with clofibrate [3].
• In summary, our results demonstrate a critical role for ACS4 and MTE-I in the hormonal regulation of steroidogenesis as a new pathway of arachidonic acid release different from the classical phospholipase A2 cascade [5].

Regulatory relationships of Acot2

• The constitutive expression of both mRNAs was low in liver, with CTE-I being expressed mainly in kidney and brown adipose tissue and MTE-I expressed in brown adipose tissue and heart [4].

Other interactions of Acot2

• Knocking down the expression of MTE-I leads to a significant reduction in the expression of steroidogenic acute regulatory protein [5].

References