Post-transcriptional regulation of glucose transporter-1 by an AU-rich element in the 3′UTR and by hnRNP A2

Griffin, Mary E.; Hamilton, Byron B.; Roy, Kristen; Du, Min; Willson, Alicia M; Keenan, Benjamin J; Wang, Xiao Wei; Nichols, Ralph C.

doi:10.1016/j.bbrc.2004.04.128

Cited by 31 publications

(24 citation statements)

References 25 publications

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“…Our previous studies show that a region of the 3′ UTR of VEGF mRNA that contains an adenosine-uridine–rich element regulates VEGF gene expression (Du et al , 2006). Our earlier reports also identified a similar AU-rich element in the 3′ UTR of GLUT1 mRNA (Griffin et al , 2004). Another report showed that the AU-rich element in human VEGF mRNA regulates gene expression in macrophages by alternating secondary structures of RNA (Ray and Fox, 2007).…”

Section: Discussionsupporting

confidence: 65%

“…Regulation by mRNA-binding proteins on 3′ UTR elements is analyzed by introducing the 3′ UTR from regulated mRNA (VEGF, GLUT1, tumor necrosis factor-α [TNF]) into the 3′ UTR of reporter genes (firefly luciferase or green fluorescent protein; Griffin et al , 2004; Du et al , 2006; Nichols et al , 2010). In this study, the 3′ UTR of VEGF was placed in the 3′ UTR of a luciferase reporter, as described previously (Du et al , 2006).…”

Section: Discussionmentioning

confidence: 99%

“…We previously identified a region of VEGF 3′ UTR that contains an AURE, and we hypothesized that the AU-rich element affected gene expression (Du et al , 2006). We identified a similar AU-rich region in the 3′ UTR of glucose transporter-1 (GLUT1) mRNA (Griffin et al , 2004). A recent report shows that the AU-rich element in human VEGF mRNA regulates gene expression by alternating secondary structures of RNA (Ray and Fox, 2007).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

AUF1/hnRNP D represses expression of VEGF in macrophages

Fellows

Griffin

Petrella

et al. 2012

MBoC

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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AUF1/hnRNP D represses expression of VEGF in macrophages

Fellows

Griffin

Petrella

et al. 2012

MBoC

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“…It has been documented that posttranscriptional regulatory mechanisms, specifically modulation of mRNA stability, can play a major role in gene expression. In many cases, it has been proven that mRNA turnover depends on mRNA binding proteins that specifically recognize adenosine uridine (AU)-rich elements or other sequence motifs in the 3′-untranslated region (3′-UTR), and either suppress or favor RNase degradation (Garayoa et al 2003;Griffin et al 2004). In accord with previous studies, hnRNP A2 has also been shown to bind to 3′-UTR AU-rich elements of glucose transporter-1 mRNA and to mediate its rapid decay under ischemic or hypoglycemic conditions (Garayoa et al 2003;He et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Histochemical Mapping of hnRNP A2/B1 in Rat Brain After Ischemia–Reperfusion Insults

Liu

Gao

et al. 2010

J Histochem Cytochem.

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Cerebral ischemia-reperfusion (I/R) insults result in neuronal cell death, brain tissue loss, and severe neurological deficits. However, the underlying mechanism is still not fully understood. Heterogeneous nuclear ribonucleoprotein (hnRNP) A2/B1 belongs to a family of RNA-binding proteins that plays a central role in pre-mRNA processing. Recent studies have revealed that hnRNP A2/B1 may be involved in the progress of I/R; therefore, the present study aimed to examine expression patterns of hnRNP A2/B1 to better understand posttranscriptional regulations in cerebral I/R insults. Focal cerebral I/R models were induced by right middle cerebral artery occlusion (MCAO) for 120 min followed by 3, 6, 12, 24, 48, and 72 hr of reperfusion in male Sprague-Dawley rats. We employed immunohistochemistry to examine expression of hnRNP A2/B1 in rat cerebral cortex (including cingulate cortex, striate cortex, temporal cortex, and piriform cortex) and hippocampus after I/R insults. Results showed that expression of hnRNP A2/B1 was significantly downregulated in cerebral cortex and hippocampus from 3 to 24 hr of reperfusion after MCAO for 120 min, but significantly upregulated at 48 hr of reperfusion. Unexpectedly, translocation of hnRNP A2/B1 from nucleus to cytoplasm and even to neurites was observed in cerebral cortex at 3 hr of reperfusion, reaching a peak at 24 hr of reperfusion, but not in hippocampus, indicating different posttranscriptional regulation patterns in different brain regions. Interestingly, translocation of hnRNP A2/B1 was only observed in cerebral cortex with MCAO but not in the opposite side, suggesting an I/R-specific expression pattern in the brain. Our data suggest that hnRNP A2/B1 participates in posttranscriptional regulation of neurons in cerebral cortex and hippocampus that suffered I/R insults, although posttranscriptional regulation is more extensive in neuronal cells of cerebral cortex than in hippocampus.

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“…The mRNA stability is mostly regulated via 3'UTR, especially by elements rich in AU repeats -ARE (AU -Rich Elements) (Griffin et al, 2004). AREs are classified into 3 groups depending on AUUUA repetitive units, regulation mechanisms and degradation efficiency.…”

Section: Transcript Stabilitymentioning

confidence: 99%

The Role of Single Nucleotide Polymorphisms of Untranslated Regions (Utrs) in Insulin Resistance Pathogenesis in Patients with Type 2 Diabetes

Małodobra¹

2011

Medical Complications of Type 2 Diabetes

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Post-transcriptional regulation of glucose transporter-1 by an AU-rich element in the 3′UTR and by hnRNP A2

Cited by 31 publications

References 25 publications

AUF1/hnRNP D represses expression of VEGF in macrophages

AUF1/hnRNP D represses expression of VEGF in macrophages

Histochemical Mapping of hnRNP A2/B1 in Rat Brain After Ischemia–Reperfusion Insults

The Role of Single Nucleotide Polymorphisms of Untranslated Regions (Utrs) in Insulin Resistance Pathogenesis in Patients with Type 2 Diabetes

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