DCAKD

Official Full Name

dephospho-CoA kinase domain containing

Organism

Homo sapiens

GeneID

79877

Background

Enables dephospho-CoA kinase activity. Predicted to be involved in coenzyme A biosynthetic process. Located in membrane. [provided by Alliance of Genome Resources, Feb 2025]

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Detailed Information

The Dephospho-CoA kinase domain containing (DCAKD) family of genes represents a class of proteins with crucial roles in various cellular processes, including metabolism, signal transduction, and cell proliferation. These genes encode proteins with important biological functions.

Structure And function of DCAKD

The DCAKD gene family encodes proteins that contain a conserved catalytic domain, which is responsible for the phosphorylation of various substrates. This domain is highly similar to the kinase domain found in other protein kinases, including serine/threonine kinases and protein tyrosine kinases. The DCAKD proteins are classified into two subfamilies, DCAKD-alpha and DCAKD-beta, based on their sequence similarities and structural features.

The DCAKD proteins are involved in a variety of cellular processes, including metabolism, signal transduction, and cell proliferation. For example, DCAKD-alpha is involved in the regulation of fatty acid metabolism and plays a role in the activation of acetyl-CoA carboxylase, a key enzyme in fatty acid synthesis. DCAKD-beta, on the other hand, is involved in the regulation of glycolysis and plays a role in the activation of hexokinase, a key enzyme in glucose metabolism.

DCAKD-related Signaling Pathways

The activity of DCAKD genes is regulated by various mechanisms, including transcriptional regulation, post-translational modification, and interaction with other cellular proteins. The transcription of DCAKD genes is controlled by various transcription factors, including nuclear receptors, MYC, and AP-1. The activity of DCAKD proteins is also regulated by post-translational modifications, such as phosphorylation and acetylation. For example, DCAKD-alpha is phosphorylated by various protein kinases, including protein kinase A and protein kinase C, which modulate its activity and substrate specificity.

DCAKD genes are also involved in various signaling pathways, including the mitogen-activated protein kinase (MAPK) pathway, the nuclear factor-κB (NF-κB) pathway, and the Wnt signaling pathway. For example, DCAKD-alpha is activated by mitogens and growth factors, which leads to the phosphorylation of its substrates and the regulation of cellular metabolism. Similarly, DCAKD-beta is activated by insulin and other hormonal signals, which leads to the activation of glycolysis and the synthesis of glycogen in liver and muscle cells.

DCAKD and Diabetes

The Dephospho-CoA kinase domain containing (DCAKD) gene plays a crucial role in the pathophysiology of diabetes. Diabetes is a metabolic disorder characterized by elevated blood glucose levels due to defects in insulin secretion or insulin action. DCAKD is an enzyme involved in the regulation of lipid metabolism, which is significantly altered in diabetes. The DCAKD gene encodes a protein with kinase activity that phosphorylates dephospho-CoA, a crucial cofactor in various metabolic pathways. Studies have shown that mutations in the DCAKD gene can lead to impaired insulin secretion and insulin resistance, which are hallmarks of diabetes. These mutations can cause defects in lipid metabolism, leading to insulin resistance and decreased glucose uptake by cells. In recent years, increasing evidence has suggested that DCAKD plays a pivotal role in the development of diabetes. Research has shown that individuals with DCAKD mutations are at higher risk of developing diabetes compared to those without these mutations. Moreover, inhibition of DCAKD activity has been shown to improve insulin sensitivity and glucose metabolism in experimental models of diabetes.

References:

Makarov, Mikhail et al. "Enzyme catalysis prior to aromatic residues: Reverse engineering of a dephospho-CoA kinase." Protein science: a publication of the Protein Society vol. 30,5 (2021): 1022-1034. doi:10.1002/pro.4068
Zhyvoloup, Alexander et al. "Molecular cloning of CoA Synthase. The missing link in CoA biosynthesis." The Journal of biological chemistry vol. 277,25 (2002): 22107-10. doi:10.1074/jbc.C200195200

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