A gene activated in mouse 3T3 cells by serum growth factors encodes a protein with "zinc finger" sequences.

Christy, Barbara A.; Lau, Lester F.; Nathans, Daniel

doi:10.1073/pnas.85.21.7857

Cited by 644 publications

(387 citation statements)

References 47 publications

Supporting

Mentioning

378

Contrasting

Unclassified

Order By: Relevance

“…Expression of Egr1 is rapidly induced by mitogens, insulin and glucose in different cells, including beta cells [19,20,34,35]. In our experiments, the rapid and transient induction of EGR1 protein in response to exendin-4 ( Fig.…”

Section: Discussionsupporting

confidence: 53%

See 1 more Smart Citation

Upregulation of rat Ccnd1 gene by exendin-4 in pancreatic beta cell line INS-1: interaction of early growth response-1 with cis-regulatory element

Kang

Kim

et al. 2006

Diabetologia

View full text Add to dashboard Cite

Aims/hypothesis: The aim of this study was to investigate the effect of exendin-4 on the expression of cyclin D1 gene (Ccnd1), which is critical in regulating the progression of the cell cycle in INS-1 cells. Materials and methods: INS-1 cells were stimulated with exendin-4 (10 nmol/l). Transient transfection and luciferase reporter assays were performed to measure promoter activities of rat Ccnd1. Electrophoretic mobility shift and chromatin immunoprecipitation assays were used to examine the binding of transcription factors to sites responsive to exendin-4 in vitro and in vivo, respectively. Results: Exendin-4 increased both Ccnd1 mRNA and its protein levels in a time-dependent manner. The region from −174 to +130 of the promoter was found to contain cis-regulatory elements responsible for exendin-4-mediated gene induction. Early growth response-1 (EGR1) protein was bound to the region from −153 to −134, which includes the putative EGR1 binding site (5′-CACCCCCGC-3′). Moreover, exendin-4 recruited EGR1 protein to the promoter in vivo. Conclusions/ interpretation: These findings suggest that exendin-4 activates Ccnd1 transcription through induction of EGR1 binding to a cis-regulatory element between −153 and −134 on the rat Ccnd1 promoter. These results provide an important indication that exendin-4 is a growth factor regulating beta cell proliferation.

show abstract

Section: Discussionsupporting

confidence: 53%

“…8a). EGR1 is an immediateearly response protein that is newly synthesised upon stimulation [19,20]. Thus, for the interaction of EGR1 with the Ccnd1 promoter, de novo EGR1 protein synthesis is required.…”

Section: Effect Of Exendin-4 On Egr1 Production In Ins-1 Cells and Prmentioning

confidence: 99%

Upregulation of rat Ccnd1 gene by exendin-4 in pancreatic beta cell line INS-1: interaction of early growth response-1 with cis-regulatory element

Kang

Kim

et al. 2006

Diabetologia

View full text Add to dashboard Cite

show abstract

“…The zinc finger backbone used to construct Jazz is related to the Zif268 gene product. 34 The Jazz DNA binding specificity has been assigned on the basis of the available list of 'code' signatures that relate zinc finger primary structure to potential nine base pair DNA binding targets. Each finger domain appears to behave as an independent DNA binding module, specifying three base pairs in adjacent but discrete subsites, essentially on one DNA strand.…”

Section: Resultsmentioning

confidence: 99%

“…The construction of Jazz gene was performed as described by Corbi et al 5,7 Briefly, following as a model the three zinc-finger peptides backbone of Zif268 protein, 34 we synthesized two overlapping oligonucleotides, named Jazz-5Ј (153 nt) and Jazz-3Ј (160 nt), respectively. Using a 20 nt long overlapping region, 5 g of each oligonucleotide was annealed, in a total volume of 50 l in the following buffer: 10 mm Tris-HCl (pH 7.5), 5 mm MgCl 2 , and 7.5 mm DTT.…”

Section: Construction Of Jazz Genementioning

confidence: 99%

The artificial zinc finger coding gene ‘Jazz’ binds the utrophin promoter and activates transcription

Corbi

Libri

Fanciulli³

et al. 2000

Gene Ther

View full text Add to dashboard Cite

“…For example, while c-FOS/c-JUN dimers are efficient activators of promotors containing AP-l sites, c-JUN/JUN B complexes seem to repress them under certain cir cumstances (Chiu et aL, 1989;Schutte et aL, 1989). KROX-24 (also termed NGFl-A [Milbrandt, 1987], EGR-l , Zif/268 [Christy et aL, 1988]) and KROX-20 (also termed EGR-2 [Jo seph et al, 1988]) belong to a family of DNA binding proteins with zinc finger motifs (Klug and Rhodes, 1987;Evans and Hollenberg, 1988). Simi lar to different FOS/JUN dimers, these zinc finger proteins compete for a specific DNA site, the so called early growth response (EGR) consensus se quence (Christy and Nathans, .…”

Section: Krox -24mentioning

confidence: 99%

Hypoglycemia-Elicited Immediate Early Gene Expression in Neurons and Glia of the Hippocampus: Novel Patterns of FOS, JUN, and KROX Expression following Excitotoxic Injury

Gass

Katsura

Zuschratter

et al. 1995

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

In the hippocampus there is a graded vulnerability of neuronal subpopulations to hypoglycemia-induced degeneration, most likely due to excitotoxic activation of glutamate receptors. The present study was conducted to investigate whether the induction of transcription factors of the immediate early gene (IEG) family after hypoglycemia reflects these different grades of neuronal vulnerability. We studied the expression profile of seven IEG-coded proteins in the rat hippocampus following severe insulin-induced hypoglycemia with 30 min of EEG isoelectricity and various survival periods for up to 42 h after glucose replenishment. Immunocytochemistry was performed on vibratome sections with specific polyclonal antisera directed against c-FOS, FOS B, c-JUN, JUN B, JUN D, KROX-24, and KROX-20. To unequivocally define the type of glial cells showing IEG induction, we investigated coexpression of c-FOS and glial marker proteins (glial fibrillary acid protein [GFAP], OX-42) by confocal laser scanning microscopy. Up to 3 h after glucose replenishment, differential temporospatial induction of IEG-coded transcription factors of the FOS, JUN and KROX families were observed in moderately injured neuronal subpopulations, including the majority of dentate granule cells and CA3 neurons. At later time points, however, a delayed and persistent c-JUN expression was found in severely, but reversibly, injured CA1 neurons and in neurons in the immediate vicinity of irreversibly damaged neurons in the crest of the dentate gyrus. Similar to the results with experimental models of central and peripheral axotomy, selective c-JUN induction in these neurons may represent an initial event in the regeneration process of sublethally injured neurons. In contrast to other models of excitotoxic injury such as ischemia and epilepsy, marked glial c-FOS expression was restricted to astrocytes, as assessed by confocal laser scanning microscopy.

show abstract

A gene activated in mouse 3T3 cells by serum growth factors encodes a protein with "zinc finger" sequences.

Cited by 644 publications

References 47 publications

Upregulation of rat Ccnd1 gene by exendin-4 in pancreatic beta cell line INS-1: interaction of early growth response-1 with cis-regulatory element

Upregulation of rat Ccnd1 gene by exendin-4 in pancreatic beta cell line INS-1: interaction of early growth response-1 with cis-regulatory element

The artificial zinc finger coding gene ‘Jazz’ binds the utrophin promoter and activates transcription

Hypoglycemia-Elicited Immediate Early Gene Expression in Neurons and Glia of the Hippocampus: Novel Patterns of FOS, JUN, and KROX Expression following Excitotoxic Injury

Contact Info

Product

Resources

About