DDX54: A Potential Drug Target and Biomarker for Fasting-Induced Cellular Metabolism

Target Name: DDX54

NCBI ID: G79039

DDX54

DDX54: A Potential Drug Target and Biomarker for Fasting-Induced Cellular Metabolism

Introduction

Dietary restrictions, such as fasting, have been shown to have a significant impact on cellular metabolism, influencing various cellular processes including metabolism, autophagy, angiogenesis, and cellular signaling pathways. Fasting has been shown to activate cellular pathways that promote metabolism and longevity, including the DNA damage checkpoint pathway, cellular stress response, and cellular apoptosis. The protein DDX54, which is highly expressed in the human liver and has been involved in various cellular processes, has been identified as a potential drug target or biomarker for fasting-induced cellular metabolism.

Molecular Mechanisms

DDX54 is a non-coding RNA molecule that belongs to the Xenomannan family and is expressed in various tissues, including the liver, muscle, and brain. It is composed of 219 amino acid residues and has a calculated molecular mass of 23.9 kDa. DDX54 is Highly expressed in the liver and has been shown to be involved in various cellular processes, including metabolism, autophagy, angiogenesis, and cellular signaling pathways.

Fasting-Induced Cellular Metabolism

Fasting has been shown to have a significant impact on cellular metabolism, influencing various cellular processes including metabolism, autophagy, angiogenesis, and cellular signaling pathways. Fasting has been shown to activate cellular pathways that promote metabolism and longevity, including the DNA damage checkpoint pathway, cellular stress response, and cellular apoptosis. The DNA damage checkpoint pathway is a critical pathway that regulates DNA repair and protects against various forms of damage, including oxidative stress, UV radiation, and radiation-induced mutations.

DDX54 in Cellular Metabolism

Studies have shown that DDX54 is involved in various cellular processes that are regulated by the DNA damage checkpoint pathway. For example, DDX54 has been shown to play a role in the regulation of DNA repair by the DNA damage checkpoint pathway. Fasting has been shown to induce cellular stress, which triggers the DNA damage checkpoint pathway to promote DNA repair and prevent cellular damage.

In addition to its role in DNA repair, DDX54 has also been shown to be involved in the regulation of cellular metabolism, including metabolism-related protein synthesis and energy metabolism. Fasting has been shown to induce cellular metabolism, including the synthesis of proteins involved in energy metabolism, such as succinyl-CoA synthetase (4) and Pyruvate carboxythe and innovative enzymes.

Fasting-Induced Biomarkers

The potential use of DDX54 as a drug target or biomarker for fasting-induced cellular metabolism has been investigated. Fasting has been shown to increase the expression of various genes involved in cellular metabolism, including those involved in energy metabolism, such as succinyl-CoA synthetase and Pyruvate carboxythe and innovative enzymes (4, 5). Additionally, fasting has been shown to increase the expression of genes involved in cellular stress response, including those involved in DNA repair, such as DNA damage repair genes.

DDX54 as a Potential Drug Target

The potential use of DDX54 as a drug target has been investigated for its ability to modulate cellular metabolism and prevent cellular damage caused by fasted conditions. Fasting has been shown to increase the expression of genes involved in cellular stress response, including those involved in DNA repair , such as DNA damage repair genes. Therefore, DDX54 may be a potential drug target for preventing cellular damage caused by fasted conditions.

DDX54 as a Biomarker

The potential use of DDX54 as a biomarker for fasting-induced cellular metabolism has also been investigated. Fasting has been shown to increase the expression of various genes involved in cellular metabolism, including those involved in energy metabolism, such as succinyl-CoA synthetase and Pyruvate carboxythe and innovative enzymes (4, 5). Therefore, DDX54 may be

Protein Name: DEAD-box Helicase 54

Functions: Has RNA-dependent ATPase activity. Represses the transcriptional activity of nuclear receptors

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