DEPTOR

Official Full Name

DEP domain containing MTOR interacting protein

Organism

Homo sapiens

GeneID

64798

Background

Enables phosphatidic acid binding activity and protein serine/threonine kinase inhibitor activity. Involved in several processes, including negative regulation of TOR signaling; negative regulation of cell size; and negative regulation of protein kinase activity. Is active in lysosomal membrane. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

DEP.6; DEPDC6; hDEPTOR;

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Detailed Information

DEPTOR, a novel protein discovered relatively recently, has garnered significant attention for its crucial role in regulating cellular homeostasis. The name DEPTOR is derived from its domain composition, which includes a DEP domain and a TOR (Target of Rapamycin) interaction domain. This protein has been found to play a vital part in various cellular processes, including cell growth, metabolism, and survival.

Function of DEPTOR

DEPTOR is a multifunctional protein that interacts with several key cellular signaling pathways. One of its primary functions is to regulate the activity of mTOR (mammalian Target of Rapamycin), a kinase that plays a critical role in cell growth and metabolism. DEPTOR binds to mTOR and inhibits its kinase activity, thereby preventing uncontrolled cell growth and promoting cellular homeostasis.

In addition to its role in regulating mTOR, DEPTOR also interacts with other proteins involved in cell signaling. For instance, it has been found to bind to and inhibit the activity of AKT, a kinase involved in cell survival and proliferation. By inhibiting AKT activity, DEPTOR helps maintain the balance between cell growth and apoptosis (cell death), ensuring that cells do not undergo uncontrolled proliferation.

Regulation of DEPTOR

The expression and activity of DEPTOR are tightly regulated by various factors, including transcriptional and post-translational mechanisms. Several studies have shown that DEPTOR expression can be upregulated by certain transcription factors, such as p53 and FOXO, which are involved in cell cycle regulation and stress responses. This suggests that DEPTOR may play a role in responding to cellular stress and maintaining genomic stability.

Moreover, DEPTOR activity is also regulated by post-translational modifications, such as phosphorylation and ubiquitination. Phosphorylation of DEPTOR on specific residues can modulate its interaction with mTOR and AKT, thereby regulating its inhibitory effects on these kinases. Ubiquitination, on the other hand, can target DEPTOR for degradation, thereby regulating its protein levels and activity.

Implications of DEPTOR in Disease

Given its role in maintaining cellular homeostasis, it is not surprising that DEPTOR has been implicated in various diseases, including cancer and metabolic disorders. In cancer, the deregulation of DEPTOR expression or function can lead to uncontrolled cell growth and proliferation, resulting in tumor formation. Similarly, in metabolic disorders, such as obesity and diabetes, the altered activity of DEPTOR can contribute to abnormal energy metabolism and insulin resistance.

Chronic alcohol consumption leads to SIRT1 inhibition in hepatocytes, which is associated with downregulation of DEPTOR and activation of mTORC1 and S6K1. Aberrant activation of mTORC1 by alcohol stimulates protein hydrolytic processing, nuclear translocation and transcriptional activity of SREBP-1, Alcohol-induced aberrant activation of mTORC1 stimulated the protein hydrolytic processing, nuclear translocation and transcriptional activity of SREBP-1, promoted the cytoplasmic translocation of lipoprotein 1, and inhibited the transcriptional activity of PPARα, which increased fatty acid synthesis and decreased fatty acid oxidation. Alcohol-induced hepatic lipogenesis is mediated by both S6K1-dependent and independent pathways. Alcohol intake mainly acts on hepatocytes through inhibition of SIRT1 and activation of mTORC1, inducing excessive fat accumulation and apoptosis.

Figure 1. SIRT1-DEPTOR-mTORC1 axis in the pathogenesis of ALD

References:

Chen H, Shen F, Sherban A, et al. DEP domain-containing mTOR-interacting protein suppresses lipogenesis and ameliorates hepatic steatosis and acute-on-chronic liver injury in alcoholic liver disease. Hepatology. 2018;68(2):496-514. doi:10.1002/hep.29849
Caron A, Baraboi ED, Laplante M, Richard D. DEP domain-containing mTOR-interacting protein in the rat brain: distribution of expression and potential implication. J Comp Neurol. 2015;523(1):93-107. doi:10.1002/cne.23668

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