What does mTOR kinase do?

What does mTOR kinase do?

In particular, as a core component of both complexes, mTOR functions as a serine/threonine protein kinase that regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, autophagy, and transcription.

What is mTOR phosphorylation?

Abstract. The mammalian target of rapamycin (mTOR) coordinates cell growth with the growth factor and nutrient/energy status of the cell. The phosphatidylinositol 3-kinase-AKT pathway is centrally involved in the transmission of mitogenic signals to mTOR.

What is mTOR autophagy?

Autophagy is a process of self-degradation that enables the cell to survive when faced with starvation or stressful conditions. The mechanistic target of rapamycin (mTOR), also known as the mammalian target of rapamycin, plays a critical role in maintaining a balance between cellular anabolism and catabolism.

What effect does mTOR have on S6K?

S6K and 4EBP regulate translational initiation and control protein synthesis. Activation of S6K by mTOR is followed by phosphorylation of a downstream ribosomal protein, S6, at serine 235/236, an alternative marker for mTOR activity, to promote protein translation (Fingar et al., 2004; Hay and Sonenberg, 2004).

How does mTOR inhibit autophagy?

mTORC1 tightly regulates autophagy by suppressing autophagy induction via phosphorylation-dependent inhibition of ULK1/2 and the VPS34 complex and by preventing global expression of lysosomal and autophagy genes through TFEB phosphorylation.

What happens when mTOR is activated?

Activation of mTOR complex 1 (mTORC1) is triggered by oxidative stress, amino-acid levels and endosomal traffic to the lysosome by small GTPases such as Rab4A. In turn, mTORC1 promotes inflammation by skewing T-cell development.

What is the mTOR signaling pathway?

The mTOR signaling pathway, which is often activated in tumors, not only regulates gene transcription and protein synthesis to regulate cell proliferation and immune cell differentiation but also plays an important role in tumor metabolism.

Does mTOR promote autophagy?

mTOR promotes anabolic metabolism and inhibits autophagy induction. Therefore, the regulation of autophagy with mTOR inhibitors provides a new therapeutic strategy for a variety of diseases, including neurodegenerative diseases, diabetes, and cancer.

Does mTOR increase aging?

A growing list of evidence suggests that mTOR signaling influences longevity and aging. Inhibition of the mTOR complex 1 (mTORC1) with rapamycin is currently the only known pharmacological treatment that increases lifespan in all model organisms studied.

What is P70S6K1?

The P70 ribosomal protein S6 kinase 1 (P70S6K1) is activated by the mammalian target of rapamycin (mTORC1) and regulates proliferation, growth, and metabolism. PF-4708671 is a novel, cell-permeable, has been proposed to be a highly specific inhibitor of p70S6K1.

What does S6K1 mean?

Ribosomal protein S6 kinase beta-1 ( S6K1 ), also known as p70S6 kinase ( p70S6K, p70-S6K ), is an enzyme (specifically, a protein kinase) that in humans is encoded by the RPS6KB1 gene. It is a serine/threonine kinase that acts downstream of PIP3 and phosphoinositide-dependent kinase-1 in the PI3 kinase pathway.

Does S6K1 interact with CoA synthase in the mTOR pathway?

“Specific interaction between S6K1 and CoA synthase: a potential link between the mTOR/S6K pathway, CoA biosynthesis and energy metabolism”. FEBS Letters. 578 (3): 357–62. doi: 10.1016/j.febslet.2004.10.091.

How does mTOR activate p70S6K?

Once mTOR has been properly localized and activated, it can phosphorylate downstream targets such as p70S6K, 4EBP, and ULK1 which are important for regulating protein anabolic/catabolic balance. Physical exercise activates protein synthesis via phosphorylation (activation) of p70S6K in a pathway that is dependent on mTOR, specifically mTORC1.

How does the mTOR pathway control CTPS cytoophidium Assembly?

Thus, these data suggest that the mTOR pathway controls CTPS cytoophidium assembly mainly through S6K1 kinase and S6K1 may directly phosphorylate CTPS and regulate its filamentation. Open in a separate window Fig. 5 mTORC1 controls CTPS cytoophidium formation through S6K1.

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