scholarly journals Rrp6 Moonlights in an RNA Exosome-Independent Manner to Promote Cell Survival and Gene Expression during Stress

Cell Reports ◽  
2020 ◽  
Vol 31 (10) ◽  
pp. 107754
Author(s):  
Charles Wang ◽  
Yanru Liu ◽  
Samuel M. DeMario ◽  
Igor Mandric ◽  
Carlos Gonzalez-Figueroa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Survival ◽  
Independent Manner ◽  
Promote Cell Survival ◽  
Rna Exosome

scholarly journals Post-transcriptional regulation by the exosome complex is required for cell survival and forebrain development via repression of P53 signaling

Development ◽  
2021 ◽  
Vol 148 (3) ◽  
pp. dev188276
Author(s):  
Pauline Antonie Ulmke ◽  
Yuanbin Xie ◽  
Godwin Sokpor ◽  
Linh Pham ◽  
Orr Shomroni ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Development ◽  
Cell Survival ◽  
Rna Stability ◽  
Rna Decay ◽  
Cortical Cells ◽  
Forebrain Development ◽  
P53 Signaling ◽  
Rna Exosome ◽  
Exosome Complex

ABSTRACTFine-tuned gene expression is crucial for neurodevelopment. The gene expression program is tightly controlled at different levels, including RNA decay. N6-methyladenosine (m6A) methylation-mediated degradation of RNA is essential for brain development. However, m6A methylation impacts not only RNA stability, but also other RNA metabolism processes. How RNA decay contributes to brain development is largely unknown. Here, we show that Exosc10, a RNA exonuclease subunit of the RNA exosome complex, is indispensable for forebrain development. We report that cortical cells undergo overt apoptosis, culminating in cortical agenesis upon conditional deletion of Exosc10 in mouse cortex. Mechanistically, Exosc10 directly binds and degrades transcripts of the P53 signaling-related genes, such as Aen and Bbc3. Overall, our findings suggest a crucial role for Exosc10 in suppressing the P53 pathway, in which the rapid turnover of the apoptosis effectors Aen and Bbc3 mRNAs is essential for cell survival and normal cortical histogenesis.

scholarly journals Akt/Protein Kinase B Inhibits Cell Death by Preventing the Release of Cytochrome c from Mitochondria

1999 ◽  
Vol 19 (8) ◽  
pp. 5800-5810 ◽  
Author(s):  
Scott G. Kennedy ◽  
Eugene S. Kandel ◽  
Torry K. Cross ◽  
Nissim Hay
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Inner Mitochondrial Membrane ◽  
Serine Threonine Kinase ◽  
Independent Manner ◽  
Akt Activation ◽  
Threonine Kinase ◽  
Promote Cell Survival ◽  
Steady State Levels ◽  
Phosphoinositide 3 Kinase

ABSTRACT Growth factors signaling through the phosphoinositide 3-kinase/Akt pathway promote cell survival. The mechanism by which the serine/threonine kinase Akt prevents cell death remains unclear. We have previously shown that Akt inhibits the activity of DEVD-targeted caspases without changing the steady-state levels of Bcl-2 and Bcl-xL. Here we show that Akt inhibits apoptosis and the processing of procaspases to their active forms by delaying mitochondrial changes in a caspase-independent manner. Akt activation is sufficient to inhibit the release of cytochrome c from mitochondria and the alterations in the inner mitochondrial membrane potential. However, Akt cannot inhibit apoptosis induced by microinjection of cytochrome c. We also demonstrated that Akt inhibits apoptosis and cytochrome c release induced by several proapoptotic Bcl-2 family members. Taken together, our results show that Akt promotes cell survival by intervening in the apoptosis cascade before cytochrome c release and caspase activation via a mechanism that is distinct from Bad phosphorylation.

scholarly journals A gene expression signature associated with ‘‘K-Ras addiction’’ reveals regulators of EMT and tumor cell survival

Cancer Cell ◽  
2021 ◽  
Vol 39 (3) ◽  
pp. 441-442
Author(s):  
Anurag Singh ◽  
Patricia Greninger ◽  
Daniel Rhodes ◽  
Louise Koopman ◽  
Sheila Violette ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Cell ◽  
Cell Survival ◽  
Gene Expression Signature ◽  
Expression Signature ◽  
Tumor Cell Survival

Kinase cascades regulating entry into apoptosis

1997 ◽  
Vol 61 (1) ◽  
pp. 33-46
Author(s):  
P Anderson
Keyword(s):  
Cell Death ◽  
Cell Surface ◽  
Cell Survival ◽  
Tyrosine Kinases ◽  
Uv Light ◽  
Apoptotic Cell ◽  
Paracrine Factors ◽  
Surface Receptors ◽  
Promote Cell Survival ◽  
Necrosis Factor

All cells are constantly exposed to conflicting environment cues that signal cell survival or cell death. Survival signals are delivered by autocrine or paracrine factors that actively suppress a default death pathway. In addition to survival factor withdrawal, cell death can be triggered by environmental stresses such as heat, UV light, and hyperosmolarity or by dedicated death receptors (e.g., FAS/APO-1 and tumor necrosis factor [TNF] receptors) that are counterparts of growth factor or survival receptors at the cell surface. One of the ways that cells integrate conflicting exogenous stimuli is by phosphorylation (or dephosphorylation) of cellular constituents by interacting cascades of serine/threonine and tyrosine protein kinases (and phosphatases). Survival factors (e.g., growth factors and mitogens) activate receptor tyrosine kinases and selected mitogen-activated, cyclin-dependent, lipid-activated, nucleic acid-dependent, and cyclic AMP-dependent kinases to promote cell survival and proliferation, whereas environmental stress (or death factors such as FAS/APO-1 ligand and TNF-alpha) activates different members of these kinase families to inhibit cell growth and, under some circumstances, promote apoptotic cell death. Because individual kinase cascades can interact with one another, they are able to integrate conflicting exogenous stimuli and provide a link between cell surface receptors and the biochemical pathways leading to cell proliferation or cell death.

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