VHL suppresses autophagy and tumor growth through PHD1-dependent Beclin1 hydroxylation.

The Von Hippel-Lindau (VHL) protein, which is frequently mutated in clear-cell renal cell carcinoma (ccRCC), is a master regulator of hypoxia-inducible factor (HIF) that is involved in oxidative stresses. However, whether VHL possesses HIF-independent tumor-suppressing activity remains largely unclear. Here, we demonstrate that VHL suppresses nutrient stress-induced autophagy, and its deficiency in sporadic ccRCC specimens is linked to substantially elevated levels of autophagy and correlates with poorer patient prognosis.

Creatine kinase B suppresses ferroptosis by phosphorylating GPX4 through a moonlighting function.

Activation of receptor protein kinases is prevalent in various cancers with unknown impact on ferroptosis. Here we demonstrated that AKT activated by insulin-like growth factor 1 receptor signalling phosphorylates creatine kinase B (CKB) T133, reduces metabolic activity of CKB and increases CKB binding to glutathione peroxidase 4 (GPX4). Importantly, CKB acts as a protein kinase and phosphorylates GPX4 S104.

Nucleus-exported CLOCK acetylates PRPS to promote de novo nucleotide synthesis and liver tumour growth.

Impairment of the circadian clock is linked to cancer development. However, whether the circadian clock is modulated by oncogenic receptor tyrosine kinases remains unclear. Here we demonstrated that receptor tyrosine kinase activation promotes CK2-mediated CLOCK S106 phosphorylation and subsequent disassembly of the CLOCK-BMAL1 dimer and suppression of the downstream gene expression in hepatocellular carcinoma (HCC) cells.

Fructose-1,6-bisphosphatase 1 functions as a protein phosphatase to dephosphorylate histone H3 and suppresses PPARα-regulated gene transcription and tumour growth.

Tumour cells exhibit greater metabolic plasticity than normal cells and possess selective advantages for survival and proliferation with unclearly defined mechanisms. Here we demonstrate that glucose deprivation in normal hepatocytes induces PERK-mediated fructose-1,6-bisphosphatase 1 (FBP1) S170 phosphorylation, which converts the FBP1 tetramer to monomers and exposes its nuclear localization signal for nuclear translocation. Importantly, nuclear FBP1 binds PPARα and functions as a protein phosphatase that dephosphorylates histone H3T11 and suppresses PPARα-mediated β-oxidation gene expression.

The N-terminus of Sec3 is required for cell wall integrity in yeast.

The cell wall is essential for cell viability and pathogenesis of fungi. It was previously shown that the exocytosis landmark Sec3 is an effector of the cell wall integrity (CWI) master regulator Rho1 GTPase. However, disruption of the interaction between Sec3 and Rho1 did not inhibit exocytic secretion and cell growth.

Sphingolipids are required for exocyst polarity and exocytic secretion in .

Background: Exocytosis is a process by which vesicles are transported to and fused with specific areas of the plasma membrane. Although several studies have shown that sphingolipids are the main components of exocytic compartments, whether they control exocytosis process is unclear.

Results: Here, we have investigated the role of sphingolipids in exocytosis by reducing the activity of the serine palmitoyl-transferase (SPT), which catalyzes the first step in sphingolipid synthesis in endoplasmic reticulum.

Cyclin-dependent kinase-mediated phosphorylation of the exocyst subunit Exo84 in late G phase suppresses exocytic secretion and cell growth in yeast.

In eukaryotic cells, the growth rate is strictly regulated for proper progression of the cell cycle. In the budding yeast , it was previously shown that cell growth dramatically slows down when the cells start budding at the G/S transition. However, the molecular mechanism for this G/S-associated growth arrest is unclear.

[Study on nanophase anatase-rutile transition with Raman spectrum].

The nanophase anatase of different size (the average is 40 nm) was synthesized with chemical precipitation method. Transition from nanophase and microphase anatase to rutile were investigated with Raman spectrum. The result indicated that rutile characteristic peak (446 cm-1) appeared after 1 h heat preservation at 900 degrees C for microphase anatase, raising the temperature characteristic peak intensity of rutile (446,610 and 231 cm-1) continued to increase and characteristic peak of anatase (639,515 and 397 cm-1) decreased bit by bit.