Ribosome stalling during translation presents actionable cancer cell vulnerability.

Myc is a major driver of tumor initiation, progression, and maintenance. Up-regulation of Myc protein level rather than acquisition of neomorphic properties appears to underlie most Myc-driven cancers. Cellular mechanisms governing Myc expression remain incompletely defined.

Stalled translation by mitochondrial stress upregulates a CNOT4-ZNF598 ribosomal quality control pathway important for tissue homeostasis.

Translational control exerts immediate effect on the composition, abundance, and integrity of the proteome. Ribosome-associated quality control (RQC) handles ribosomes stalled at the elongation and termination steps of translation, with ZNF598 in mammals and Hel2 in yeast serving as key sensors of translation stalling and coordinators of downstream resolution of collided ribosomes, termination of stalled translation, and removal of faulty translation products. The physiological regulation of RQC in general and ZNF598 in particular in multicellular settings is underexplored.

Depression among People Living With HIV/AIDS Undergoing Antiretroviral Therapy at a Tertiary Care Centre: A Descriptive Cross-sectional Study.

Introduction: HIV affects mental health in multiple ways, including its direct pathophysiological effects, associated stigma, impacts on social, and economic dimensions, medications used for long durations and multiple secondary physical health issues that affect the clients and comorbid substance use. In the post-COVID era, in our socio-cultural and geographical context, depression among these populations needs assessment to evaluate their mental health care needs. The objective of this study was to find out the prevalence of depression among people living with HIV/AIDS undergoing antiretroviral therapy at a tertiary care centre.

Reverse electron transfer is activated during aging and contributes to aging and age-related disease.

Mechanisms underlying the depletion of NAD and accumulation of reactive oxygen species (ROS) in aging and age-related disorders remain poorly defined. We show that reverse electron transfer (RET) at mitochondrial complex I, which causes increased ROS production and NAD to NADH conversion and thus lowered NAD /NADH ratio, is active during aging. Genetic or pharmacological inhibition of RET decreases ROS production and increases NAD /NADH ratio, extending the lifespan of normal flies.