High impact information on Egr2

• Interestingly, Sox10 also modulated the function of Pax3 and Krox-20, two other transcription factors involved in Schwann cell development [1].
• Many of the immediate early genes (IEGs) such as c-fos, NGFI-A, NGFI-C, and Krox-20 were found to be robustly upregulated in the three different regions studied [2].
• In the present studies, insulin treatment rapidly increased transcription of both Egr-1 and Krox20 [3].
• Finally, inhibition of the p38 pathway, followed by insulin addition, caused an additive induction of both Egr-1and Krox20 [3].
• Using differential screening of H4IIE cells, we have identified two members of the Egr zinc-finger transcription factor family of early response genes, Egr-1 and Krox20, whose transcription is induced by insulin treatment [3].

Biological context of Egr2

• Krox20 may play a key role in the stabilization of long-term potentiation [4].
• The day 28 infarct zone response mirrored the day 1 remote zone response including activation of genes associated with matrix remodeling (metallothionein and metalloproteinase 9, 12, 23), as well as genes associated with cell proliferation and phenotype specification (MYC, EGR2, ATF3, HOXA1) recapitulating developmental histogenesis programs [5].

Anatomical context of Egr2

• mRNA differential display reveals Krox-20 as a neural plasticity-regulated gene in the rat hippocampus [6].
• All convulsants induced Egr-1 and Egr-2 immunoreactivity in the cerebral cortex and hippocampus [7].
• Bands composed, at least in part, of Egr-2 and Egr-3 were present in different relative amounts in the cerebral cortex, striatum, hippocampus, thalamus, and midbrain [7].
• A weak C-fiber input caused by noxious mechanical stimulation of the skin of one hindpaw did not induce expression of c-Fos, FosB, Krox-20 or Krox-24; but it did reduce the basal expressions of c-Jun and JunD in both the medial and lateral areas [8].
• An intense input produced by electrical stimulation of all the C-fibers in one sciatic nerve also failed to induce expression of c-Fos, FosB, Krox-20 or Krox-24 in the medial or lateral areas [8].

Associations of Egr2 with chemical compounds

• Krox-20 was not induced by angiotensin II [9].
• Administration of the convulsants NMDA, kainate, and pentylenetetrazole differentially induced Egr-1 and Egr-2/3 DNA-binding activities in the cerebral cortex, hippocampus, and cerebellum [7].

Other interactions of Egr2

• In addition, EE-housed rats showed considerable diurnal variation in NGFI-A, Krox-20, and NGFI-B mRNA expression which was absent in single-housed rats [10].
• MK801 pretreatment produced a very strong inhibition of Fos, Jun-D and Krox-20 increases in dentate neurons but had a much smaller effect on Jun-B and c-Jun expression [11].
• Whole-mount in situ hybridisation was used to monitor the expression domains of Otx2, Emx2, Krox20, and hoxb1 [12].
• SCIP/Oct-6, Krox-20, and desert hedgehog mRNA expression during CNS remyelination by transplanted olfactory ensheathing cells [13].
• Transdifferentiated cultivated rat MSC (tMSC) changed morphologically into cells resembling typical spindle-shaped Schwann cells (SC) with enhanced expression of LNGF receptor, Krox-20, CD104 and S100beta protein and decreased expression of bone morphogenetic protein receptor-1A compared to untreated rat MSC (rMSC) [14].

Analytical, diagnostic and therapeutic context of Egr2

• In this study, we addressed this question by using a transplantation approach to generate myelinating OECs and then examined the expression of SCIP/Oct-6 and Krox-20 mRNA by in situ hybridization using oligonucleotide probes [13].

References