Results 11 to 20 of about 7,295 (170)

Activation of Gcn2 in response to different stresses.

open access: yesPLoS ONE, 2017
All organisms have evolved pathways to respond to different forms of cellular stress. The Gcn2 kinase is best known as a regulator of translation initiation in response to starvation for amino acids.
Silje Anda   +2 more
doaj   +3 more sources

Involvement of the eIF2α Kinase GCN2 in UV-B Responses [PDF]

open access: yesFrontiers in Plant Science, 2019
GCN2 (general control nonrepressed 2) is a serine/threonine-protein kinase that regulates translation in response to stressors such as amino acid and purin deprivation, cold shock, wounding, cadmium, and UV-C exposure. Activated GCN2 phosphorylates the α-
Paula Llabata   +9 more
doaj   +4 more sources

Yeast Gcn2 retains activity following humanization of its auto-phosphorylation region. [PDF]

open access: yesFEBS Open Bio
Using Saccharomyces cerevisiae as a model to study Gcn2 activation and regulation is limited by the lack of antibodies detecting phosphorylated Gcn2. To overcome this, we engineered Gcn2‐HsC, a yeast Gcn2 variant recognizable by commercial anti‐human phospho‐GCN2 antibodies.
Anderson RA, Schiemann AH, Sattlegger E.
europepmc   +2 more sources

Multifaceted role of GCN2 in tumor adaptation and therapeutic targeting

open access: yesTranslational Oncology
Tumor cells voraciously consume nutrients from their environment to facilitate rapid proliferation, necessitating effective strategies to manage nutrient scarcity during tumor growth and progression.
Can Chen, Yaping Xie, Shenxian Qian
doaj   +3 more sources

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer. [PDF]

open access: yesMol Oncol
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Kim A   +7 more
europepmc   +2 more sources

Alkylating Agent–Induced FANCL Impairment Damages Pulmonary Arterial, Venous, and Microvascular Endothelial Cells and Predisposes to PAH/PVOD [PDF]

open access: yesAdvanced science
This study establishes a novel cisplatin‐induced rat model of PAH/PVOD and identifies a conserved mechanistic axis—FANCL impairment, DNA damage accumulation, and endothelial dysfunction—triggered by cisplatin or mitomycin C across pulmonary arteries, veins, and microvessels.
Liu S   +20 more
europepmc   +2 more sources

Crystal structures of GCN2 C-terminal domain: Insight into GCN2 regulation [PDF]

open access: yesActa Crystallographica Section A Foundations and Advances, 2014
General control non-derepressible 2 kinase (GCN2) is a serine threonine kinase that curtails translation in response to diverse stress stimuli [1]. It is a primary sensor of amino acid starvation and mediates translation repression by phosphorylating eIF2 [2].
Isha Singh   +6 more
openaire   +1 more source

GCN2: roles in tumour development and progression

open access: yesBiochemical Society Transactions, 2022
GCN2 (general control nonderepessible 2) is an eIF2α kinase responsible for entirely rewiring the metabolism of cells when they are put under amino acid starvation stress. Recently, there has been renewed interest in GCN2 as a potential oncotarget, with several studies reporting the development of small molecule inhibitors.
Lyssa T. Gold, Glenn R. Masson
openaire   +3 more sources

Genetic and Pharmacological Inhibition of GCN2 Ameliorates Hyperglycemia and Insulin Resistance in Type 2 Diabetic Mice

open access: yesAntioxidants, 2022
It is well recognized that there is a strong and complex association between nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2D).
Juntao Yuan   +7 more
doaj   +1 more source

The Gcn2 Kinase as a Cell Cycle Regulator [PDF]

open access: yesCell Cycle, 2007
Cell cycle progression through G1 phase is of particular importance because this is the phase where the decision to embark on another cell cycle is made. An aberrant G1/S transition often leads to cell cycle deregulation and cancer development. Therefore, there is a complex regulatory network to ensure timely entry into S phase, coordinating initiation
Beáta, Grallert, Erik, Boye
openaire   +2 more sources

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