2005年9月23日 · The Class IA phosphatidylinositol (PI) 3-kinase plays a well recognized role in the regulation of S6K1. We now present evidence that the Class III PI 3-kinase, hVps34, also regulates S6K1, and is a critical component of the nutrient sensing apparatus.

Recent studies have shown that the nutrient input to the mTOR Complex1/S6K1 signaling pathway is mediated by class 3 PI3K or hVps34, the oldest member of the PI3K family. Moreover, studies to date would suggest that during the evolution of multicellular organisms this ancient branch of the pathway w …

2008年2月15日 · The Class III PI3K (phosphoinositide 3-kinase), Vps34 (vacuolar protein sorting 34), was first described as a component of the vacuolar sorting system in Saccharomyces cerevisiae and is the sole PI3K in yeast. The homologue in mammalian cells, hVps34, has been studied extensively in the context of e …

2007年4月1日 · hVps34 is known to play a critical role in autophagy, and has been shown to directly interact with the autophagic gene beclin. Beclin was first identified as a Bcl-2-interacting protein in a yeast two-hybrid screen [61].

Our data suggest that hVps34 is a nutrient-regulated lipid kinase that integrates amino acid and glucose inputs to mTOR and S6K1. p70 S6 kinase (S6K1) 2 regulates protein synthesis, cell size, and proliferation in response to cellular nutritional status and hormonal stimulation (1).

我们的发现凸显了hVps34-SGK3途径的重要性，并暗示了它代表了一种抑制PI3K / Akt信号转导的机制。 数据支持靶向Akt和SGK作为癌症治疗剂的潜力。 EN

2008年5月7日 · AAs appear to mediate this response through class III phosphatidylinositol 3-kinase (PI3K), or human vacuolar protein sorting 34 (hVps34), rather than through the canonical class I PI3K pathway used by growth factors and hormones.

We now present evidence that the Class III PI 3-kinase, hVps34, also regulates S6K1, and is a critical component of the nutrient sensing apparatus.

Recent studies have shown that mammalian hVps34 is required for the activation of the mTOR (mammalian target of rapamycin)/S6K1 (S6 kinase 1) pathway, which regulates protein synthesis in response to nutrient availability.

We demonstrate that the rise in [Ca 2+]i increases the direct binding of Ca 2+ /CaM to an evolutionarily conserved motif in hVps34 that is required for lipid kinase activity and increased mTOR Complex1 signaling. These findings have important implications regarding the basic signaling mechanisms linking metabolic disorders with cancer progression.