Hypoxic condition- and high cell density-induced expression of Redd1 is regulated by activation of hypoxia-inducible factor-1α and Sp1 through the phosphatidylinositol 3-kinase/Akt signaling pathway

Jin, Hyeon‐Ok; An, Sungkwan; Lee, Hyung-Chahn; Woo, Sang-Hyeok; Seo, Sung‐Keum; Choe, Taeboo; Yoo, Doo-Hyun; Lee, Seung Bum; Um, Hong‐Duck; Lee, Su‐Jae; Park, Myungjin; Kim, Jong‐Il; Hong, Seok‐Il; Rhee, Chang-Hun; Park, In-Chul

doi:10.1016/j.cellsig.2006.12.014

Cited by 84 publications

(53 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Transcriptional induction of both CHOP and TRB3 is mediated by the increased production of ATF4 in response to ER stress (22,25). Redd1 induced by coactivation of both HIF1a and Sp1 in the cells exposed to hypoxia is required for inhibition of mTOR (26,27). It has been recently reported that ATF4 is essential for Redd1 expression by ER stress (20,28).…”

Section: Nupr1 Stimulates Atf4 Transcriptional Activitymentioning

confidence: 99%

Nuclear protein 1 induced by ATF4 in response to various stressors acts as a positive regulator on the transcriptional activation of ATF4

et al. 2009

Self Cite

View full text Add to dashboard Cite

SummaryNuclear protein 1 (NUPR1) was originally identified as p8, a member of the family of HMG-I/Y transcription factors induced in response to various cellular stressors. However, the signaling pathway underlying NUPR1 induction by cellular stresses remains to be established. In this study, we found that the expression of NUPR1 by various stresses induced by activating transcription factor 4 (ATF4). Loss of ATF4 using siRNA significantly diminished NUPR1 expression. Overexpression of ATF4 caused NUPR1 levels to rise. NUPR1 expression was associated with enhanced transcriptional activation of genes of ATF4 downstream, suggesting that the protein promoted the transcription of stress-regulated genes via positive feedback on the ATF4 pathway.

show abstract

Section: Nupr1 Stimulates Atf4 Transcriptional Activitymentioning

confidence: 99%

Nuclear protein 1 induced by ATF4 in response to various stressors acts as a positive regulator on the transcriptional activation of ATF4

et al. 2009

Self Cite

View full text Add to dashboard Cite

show abstract

“…Several studies have shown that CoCl 2 induced hypoxia, which in turn activated the PI3K/Akt pathway to mediate CoCl 2 biological effects. [153][154][155] Further studies are warranted to characterize…”

Section: Change Of Nature Of Biomaterialsmentioning

confidence: 99%

The Key Regulatory Roles of the PI3K/Akt Signaling Pathway in the Functionalities of Mesenchymal Stem Cells and Applications in Tissue Regeneration

Chen

Crawford

Chen

et al. 2013

Tissue Engineering Part B: Reviews

203

161

View full text Add to dashboard Cite

Mesenchymal stem cells (MSCs) are multipotent cells that can differentiate into various cell types and have been widely used in tissue engineering application. In tissue engineering, a scaffold, MSCs and growth factors are used as essential components and their interactions have been regarded to be important for regeneration of tissues. A critical problem for MSCs in tissue engineering is their low survival ability and functionality. Most MSCs are going to be apoptotic after transplantation. Therefore, increasing MSC survival ability and functionalities is the key for potential applications of MSCs. Several approaches have been studied to increase MSC tissue forming capacity including application of growth factors, overexpression of stem cell regulatory genes, and improvement of biomaterials for scaffolds. The effects of these approaches on MSCs have been associated with activation of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. The pathway plays central regulatory roles in MSC survival, proliferation, migration, angiogenesis, cytokine production, and differentiation. In this review, we summarize and discuss the literatures related to the roles of the PI3K/Akt pathway in the functionalities of MSCs and the involvement of the pathway in biomaterials-increased MSC functionalities. Biomaterials have been modified in their properties and surface structure and loaded with growth factors to increase MSC functionalities. Several studies demonstrated that the biomaterials-increased MSC functionalities are mediated by the activation of the PI3K/Akt pathway. MSCs are going to be apoptotic after transplantation. Therefore, increasing MSC survival ability and functionalities is the key for potential applications of MSCs. Several approaches have been studied to increase MSC tissue forming capacity including application of growth factors, overexpression of stem cell regulatory genes, and improvement of biomaterials for scaffolds. The effects of these approaches on MSCs have been associated with activation of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. The pathway plays central regulatory roles in MSC survival, proliferation, migration, angiogenesis, cytokine production, and differentiation. In this review, we summarize and discuss the literatures related to the roles of the PI3K/Akt pathway in the functionalities of MSCs and the involvement of the pathway in biomaterials-increased MSC functionalities. Biomaterials have been modified in their properties and surface structure and loaded with growth factors to increase MSC functionalities. Several studies demonstrated that the biomaterials-increased MSC functionalities are mediated by the activation of the PI3K/Akt pathway.

show abstract

“…One transcriptional target of HIF1 in flies and mammals is Regulated in Development and DNA Damage Responses 1 (REDD1) [54,55,123]. REDD1 activates the TSC1/TSC2 tuberous sclerosis complex by releasing TSC2 from inhibitory 14-3-3 proteins, allowing TSC2 to interact with TSC1, resulting in TORC1 inhibition [54,55,124].…”

Section: Introductionmentioning

confidence: 99%

TOR and ageing: a complex pathway for a complex process

McCormick

Tsai

Kennedy

2011

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

Studies in invertebrate model organisms have led to a wealth of knowledge concerning the ageing process. But which of these discoveries will apply to ageing in humans? Recently, an assessment of the degree of conservation of ageing pathways between two of the leading invertebrate model organisms, Saccharomyces cerevisiae and Caenorhabditis elegans, was completed. The results (i) quantitatively indicated that pathways were conserved between evolutionarily disparate invertebrate species and (ii) emphasized the importance of the TOR kinase pathway in ageing. With recent findings that deletion of the mTOR substrate S6K1 or exposure of mice to the mTOR inhibitor rapamycin result in lifespan extension, mTOR signalling has become a major focus of ageing research. Here, we address downstream targets of mTOR signalling and their possible links to ageing. We also briefly cover other ageing genes identified by comparing worms and yeast, addressing the likelihood that their mammalian counterparts will affect longevity.

show abstract

Hypoxic condition- and high cell density-induced expression of Redd1 is regulated by activation of hypoxia-inducible factor-1α and Sp1 through the phosphatidylinositol 3-kinase/Akt signaling pathway

Cited by 84 publications

References 31 publications

Nuclear protein 1 induced by ATF4 in response to various stressors acts as a positive regulator on the transcriptional activation of ATF4

Nuclear protein 1 induced by ATF4 in response to various stressors acts as a positive regulator on the transcriptional activation of ATF4

The Key Regulatory Roles of the PI3K/Akt Signaling Pathway in the Functionalities of Mesenchymal Stem Cells and Applications in Tissue Regeneration

TOR and ageing: a complex pathway for a complex process

Contact Info

Product

Resources

About