TIGAR: A Promising Drug Target for Fructose-2,6-Bisphosphate 2-Phosphatase

Target Name: TIGAR

NCBI ID: G57103

TIGAR

TIGAR: A Promising Drug Target for Fructose-2,6-Bisphosphate 2-Phosphatase

Introduction

Fructose-2,6-bisphosphate (FBP) is a key regulator of cellular metabolism, particularly for the synthesis of macromolecules, including nucleic acids and intracellular signaling proteins. FBP is synthesized from fructose, which is a simple carbohydrate found in a wide variety of fruits and vegetables. However, the body's ability to produce and utilize FBP is limited by its rate of synthesis and degradation. As a result, cellular levels of FBP often become elevated when the body needs to synthesize or break down macromolecules, leading to a range of physiological processes, including muscle growth, bone development, and cell signaling.

TIGAR: A Potential Drug Target for FBP 2-Phosphatase

The fructose-2,6-bisphosphate 2-phosphatase (TIGAR) is a protein that is involved in the breakdown of FBP at the cellular level. TIGAR is a key enzyme in the fructose pathway, which is a critical pathway for the production of FBP from fructose. In addition, TIGAR is involved in regulating cellular levels of FBP, which helps to maintain a delicate balance of synthesis and degradation.

TIGAR's role in FBP metabolism has led to its potential as a drug target. By inhibiting TIGAR's activity, researchers can reduce the amount of FBP available in cells, which can lead to a range of therapeutic effects. These effects can include:

1. Muscle Growth and Proteostasis: FBP is a critical regulator of muscle growth and protein synthesis. In muscle fibers, FBP helps to stimulate the growth of new muscle cells and supports the maintenance of muscle mass. Inhibiting TIGAR activity can reduce the presence of FBP in cells availability, leading to reduced muscle growth and protein synthesis, treating diseases such as muscle atrophy.

2. Bone Development: FBP is also involved in regulating bone development and resorption. Inhibiting the activity of TIGAR can reduce the availability of FBP in cells, thereby leading to bone loss and treating diseases such as osteoporosis.

3. Cell Signaling: FBP is a critical regulator of cellular signaling, including the regulation of cell proliferation and differentiation. Inhibiting the activity of TIGAR can reduce the availability of FBP in cells, resulting in reduced cell signaling and the treatment of cancer and neurodegenerative diseases. and other diseases.

4. Metabolic Disorders: FBP is also involved in the regulation of cellular metabolism, including the synthesis and breakdown of macromolecules. Inhibiting the activity of TIGAR can reduce the availability of FBP in cells, thereby leading to metabolic disorders and treating diseases such as obesity and diabetes.

Conclusion

TIGAR is a protein that plays a critical role in the regulation of fructose-2,6-bisphosphate (FBP) metabolism. FBP is a key regulator of cellular metabolism, particularly for the synthesis of macromolecules. Inhibiting TIGAR activity can reduce FBP metabolism in cells The availability of these drugs leads to a series of biological effects and provides new ideas for the treatment of various diseases.

Protein Name: TP53 Induced Glycolysis Regulatory Phosphatase

Functions: Fructose-bisphosphatase hydrolyzing fructose-2,6-bisphosphate as well as fructose-1,6-bisphosphate (PubMed:19015259). Acts as a negative regulator of glycolysis by lowering intracellular levels of fructose-2,6-bisphosphate in a p53/TP53-dependent manner, resulting in the pentose phosphate pathway (PPP) activation and NADPH production (PubMed:16839880, PubMed:22887998). Contributes to the generation of reduced glutathione to cause a decrease in intracellular reactive oxygen species (ROS) content, correlating with its ability to protect cells from oxidative or metabolic stress-induced cell death (PubMed:16839880, PubMed:19713938, PubMed:23726973, PubMed:22887998, PubMed:23817040). Plays a role in promoting protection against cell death during hypoxia by decreasing mitochondria ROS levels in a HK2-dependent manner through a mechanism that is independent of its fructose-bisphosphatase activity (PubMed:23185017). In response to cardiac damage stress, mediates p53-induced inhibition of myocyte mitophagy through ROS levels reduction and the subsequent inactivation of BNIP3. Reduced mitophagy results in an enhanced apoptotic myocyte cell death, and exacerbates cardiac damage (By similarity). Plays a role in adult intestinal regeneration; contributes to the growth, proliferation and survival of intestinal crypts following tissue ablation (PubMed:23726973). Plays a neuroprotective role against ischemic brain damage by enhancing PPP flux and preserving mitochondria functions (By similarity). Protects glioma cells from hypoxia- and ROS-induced cell death by inhibiting glycolysis and activating mitochondrial energy metabolism and oxygen consumption in a TKTL1-dependent and p53/TP53-independent manner (PubMed:22887998). Plays a role in cancer cell survival by promoting DNA repair through activating PPP flux in a CDK5-ATM-dependent signaling pathway during hypoxia and/or genome stress-induced DNA damage responses (PubMed:25928429). Involved in intestinal tumor progression (PubMed:23726973)

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