Expression of a ULK1/2 binding-deficient ATG13 variant can partially restore autophagic activity in ATG13-deficient cells.

Autophagy describes an intracellular process responsible for the lysosome-dependent degradation of cytosolic components. The ULK1/2 complex comprising the kinase ULK1/2 and the accessory proteins ATG13, RB1CC1, and ATG101 has been identified as a central player in the autophagy network, and it represents the main entry point for autophagy-regulating kinases such as MTOR and AMPK. It is generally accepted that the ULK1 complex is constitutively assembled independent of nutrient supply.

Deubiquitinase inhibition by WP1130 leads to ULK1 aggregation and blockade of autophagy.

Autophagy represents an intracellular degradation process which is involved in both regular cell homeostasis and disease settings. In recent years, the molecular machinery governing this process has been elucidated. The ULK1 kinase complex consisting of the serine/threonine protein kinase ULK1 and the adapter proteins ATG13, RB1CC1, and ATG101, is centrally involved in the regulation of autophagy initiation.

PDK1 controls upstream PI3K expression and PIP3 generation.

The PI3K/PDK1/Akt signaling axis is centrally involved in cellular homeostasis and controls cell growth and proliferation. Due to its key function as regulator of cell survival and metabolism, the dysregulation of this pathway is manifested in several human pathologies including cancers and immunological diseases. Thus, current therapeutic strategies target the components of this signaling cascade.

DNA-flow cytometry, DNA-image cytometry and proliferation index (MIB-5) in irradiated rat salivary glands and salivary gland tumors.

Aim: Salivary glands (SG) can become atrophic following radiation exposure. Malignant transformation of SG in a radiation field is another known sequela of patients who have been treated by radiotherapy for a malignant tumor in the head and neck region. The aim of this study was to investigate cytogenetic alterations and to determine the proliferation index (PI) of SG of rats subjected to various total dosages of fractionated X-rays.