Crif1 is a novel transcriptional coactivator of STAT3

Kwon, Min-Chul; Koo, Bon–Kyoung; Moon, Jin-Sook; Kim, Yoon Young; Park, Ki Cheol; Kim, Nam Shik; Kwon, Mi Yi; Kong, Myung Phil; Yoon, Ki Jun; Im, Sun Kyoung; Ghim, Jaewang; Han, Yong Mahn; Jang, Sung Key; Shong, Minho; Kong, Young Yun

doi:10.1038/sj.emboj.7601986

Cited by 63 publications

(82 citation statements)

References 48 publications

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“…Indeed, many different functions have been reported for mammalian CRIF1, including functions as a transcription co-factor and functions in mitochondria. [29][30][31][32][33] We are currently investigating the functions of dCRIF and its role in Dcr-2 stability.…”

Section: Discussionmentioning

confidence: 99%

Requirement for CRIF1 in RNA interference and Dicer-2 stability

et al. 2014

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Abbreviations: CRIF1, Cytokine response 6 (CR6)-interacting factor 1; Gadd45GIP1, growth arrest and DNA-damageinducible 45-gamma interacting protein 1; Dcr-2, RNAase III enzyme Dicer-2 RNA interference (RNAi) is a eukaryotic gene-silencing system. Although the biochemistry of RNAi is relatively well defined, how this pathway is regulated remains incompletely understood. To identify genes involved in regulating the RNAi pathway, we screened for genetic mutations in Drosophila that alter the efficiency of RNAi. We identified the Drosophila homolog of the mammalian CR6-interacting factor 1 (CRIF1), also known as growth arrest and DNA-damageinducible 45-gamma interacting protein (Gadd45GIP1), as a potential new regulator of the RNAi pathway. Loss-offunction mutants of Drosophila CRIF1 (dCRIF) are deficient in RNAi-mediated target gene knock-down, in the biogenesis of small interfering RNA (siRNA) molecules, and in antiviral immunity. Moreover, we show that dCRIF may function by interacting with, and stabilizing, the RNase III enzyme Dicer-2. Our results suggest that dCRIF may play an important role in regulating the RNAi pathway.

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Section: Discussionmentioning

confidence: 99%

Requirement for CRIF1 in RNA interference and Dicer-2 stability

et al. 2014

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“…PACT-Luc and m67-Luc were, respectively, provided by Dr. Tarik Moroy (27) and Dr. Yong-Yun Kong (28). FLAG-STAT3 constructs were obtained from Dr. Darnell Jr., and GST-STAT3 was from Dr. XinMin Cao.…”

Section: Methodsmentioning

confidence: 99%

CUEDC2 (CUE Domain-containing 2) and SOCS3 (Suppressors of Cytokine Signaling 3) Cooperate to Negatively Regulate Janus Kinase 1/Signal Transducers and Activators of Transcription 3 Signaling

Zhang

Wang²,

Wang

et al. 2012

Journal of Biological Chemistry

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Background: Deactivation of the JAK1/STAT3 pathway is tightly controlled in cells. Results: CUEDC2 inhibits JAK1/STAT3 signaling through binding to SOCS3. Conclusion: CUEDC2 is a novel regulator of JAK1/STAT3 signaling. Significance: Our study identified a novel potential mechanism of SOCS3-mediated suppression on the JAK/STAT signaling pathway and provided important insight into the critical roles of CUEDC2 in the complex signal transduction network.

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“…Floxed Crif1 (Crif1 flox/flox ) mice were generated as described previously [20]. Crif1 flox/flox mice were mated with Ins2-Cre transgenic mice to produce beta cellspecific Crif1-knockout (Crif1 beta−/− mice (10 nmol/kg) by daily subcutaneous injection for 4 weeks starting at 4 weeks of age.…”

Section: Methodsmentioning

confidence: 99%

Disruption of CR6-interacting factor-1 (CRIF1) in mouse islet beta cells leads to mitochondrial diabetes with progressive beta cell failure

et al. 2015

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Aim/hypothesis Although mitochondrial oxidative phosphorylation (OxPhos) dysfunction is believed to be responsible for beta cell dysfunction in insulin resistance and mitochondrial diabetes, the mechanisms underlying progressive beta cell failure caused by defective mitochondrial OxPhos are largely unknown. Methods We examined the in vivo phenotypes of beta cell dysfunction in beta cell-specific Crif1 (also known as Gadd45gip1)-deficient mice. CR6-interacting factor-1 (CRIF1) is a mitochondrial protein essential for the synthesis and formation of the OxPhos complex in the inner mitochondrial membrane. Results Crif1beta−/− mice exhibited impaired glucose tolerance with defective insulin secretion as early as 4 weeks of age without defects in islet structure. At 11 weeks of age, Crif1 beta−/− mice displayed characteristic ultrastructural mitochondrial abnormalities as well as severe glucose intolerance. Furthermore, islet area and insulin content was decreased by approximately 50% compared with wild-type mice. Treatment with the glucoregulatory drug exenatide, a glucagon-like peptide-1 (GLP-1) agonist, was not sufficient to preserve beta cell function in Crif1 beta−/− mice. Conclusions/interpretation Our results indicate that mitochondrial OxPhos dysfunction triggers progressive beta cell failure that is not halted by treatment with a GLP-1 agonist. The Crif1 beta−/− mouse is a useful model for the study of beta cell failure caused by mitochondrial OxPhos dysfunction.

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Crif1 is a novel transcriptional coactivator of STAT3

Cited by 63 publications

References 48 publications

Requirement for CRIF1 in RNA interference and Dicer-2 stability

Requirement for CRIF1 in RNA interference and Dicer-2 stability

CUEDC2 (CUE Domain-containing 2) and SOCS3 (Suppressors of Cytokine Signaling 3) Cooperate to Negatively Regulate Janus Kinase 1/Signal Transducers and Activators of Transcription 3 Signaling

Disruption of CR6-interacting factor-1 (CRIF1) in mouse islet beta cells leads to mitochondrial diabetes with progressive beta cell failure

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