olig2 cre (Jackson Laboratory)
Structured Review

Olig2 Cre, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/olig2 cre/product/Jackson Laboratory
Average 86 stars, based on 1 article reviews
Images
1) Product Images from "PIEZOs regulate oligodendrocyte sheath formation, expansion, and myelination potential"
Article Title: PIEZOs regulate oligodendrocyte sheath formation, expansion, and myelination potential
Journal: bioRxiv
doi: 10.64898/2026.04.23.720488
Figure Legend Snippet: A. Raw images from Fura2 calcium imaging after the application of DMSO, 30 µM Yoda1, and 200 mM KCl. Scale bar: 25 μm B. Representative calcium imaging trace from control ( Piezo1 Wt/Wt ;Olig2 Cre/Wt ) OPCs loaded with Fura2 and sequentially exposed to DMSO, 30 µM Yoda1, and 200 mM KCl. Trace averaged from 72 cells imaged from 1 coverslip. C. Representative calcium imaging trace from Piezo1 CKO cells ( Piezo1 Fl/Fl ;Olig2 Cre/Wt ) loaded with Fura2 and exposed to DMSO, 30 µM Yoda1, and 200 mM KCl. Trace averaged from 121 CKO cells from a single coverslip. D. Quantification of area under the 340/380 curve for each animal during application of Yoda1. The imaging data from 3 coverslips per animal were pooled for analysis for 3 animals per genotype. Data shown as mean ± SEM. p = 0.024 by student’s t-test, N = 3 animals per genotype, 971 control cells and 1043 cells from Piezo1 CKO cells, 3 independent isolations. E. Representative images from EdU proliferation assay of control or Piezo1 CKO cells. OLIG2 is a marker of OLCs, and EdU labels cells that divided over the 6.5-hour time course. F. Experimental design for the detection of proliferating cells in vitro . G. Quantification of the proportion of OLIG2+ cells labelled for EdU. N = 3 independent OPC isolations per genotype, with 818 cells assessed for controls and 947 cells for Piezo1 CKOs . p = 0.643 by paired t-test. H. Representative images from control or Piezo1 CKO cells fixed 48 hours into differentiation and stained for OLIG2, PDGFRA, and MBP. I. Quantification of the percentage of OLIG2+ cells that are PDGFRA+ OPCs. Control experimental totals: 859 cells, 3 animals, 3 independent OPC isolations CKO experimental totals: 824 cells, 3 animals, 3 independent OPC isolations. p = 0.207 by paired, 2-tailed t-test. J. Quantification of the percentage of OLIG2+ cells that are actively differentiating (PDGFRA-, MBP-). Control experimental totals: 859 cells, 3 animals, 3 independent OPC isolations CKO experimental totals: 824 cells, 3 animals, 3 independent OPC isolations. p = 0.101 by paired, 2-tailed t-test. K. Quantification of the percentage of OLIG2+ cells that are MBP+ OLs. Control experimental totals: 859 cells, 3 animals, 3 independent OPC isolations CKO experimental totals: 824 cells, 3 animals, 3 independent OPC isolations. p = 0.097 by paired, 2-tailed t-test. L. Representative images of a control and Piezo1 CKO cell plated onto nanofibers and allowed to differentiate for 7 days before being fixed and stained with DAPI and MBP. M. The number of sheaths per OL for Control and Piezo1 CKO cells. p = 0.767 by paired, 2-tailed, t-test. N. Average sheath length per OL for Control and Piezo1 CKO cells. p = 0.019 by paired, 2-tailed t-test. O. Average myelin output (summed sheath lengths per OL) for control ( Piezo1 wt/wt ;Olig2 Cre/wt ) and Piezo1 CKO cells. p = 0.032 by paired, 2-tailed t-test. For M-O, Control experimental totals: 50 cells, 3 animals, 3 independent cell isolations. CKO experimental totals: 48 cells, 3 animals, 3 independent cell isolations. For E, H, and L – Scale bar: 50 μm
Techniques Used: Imaging, Control, Proliferation Assay, Marker, In Vitro, Staining
![Cortical architecture and oligodendroglial cell density in Emx1‐Cre‐mediated Slc35a2 conditional knockout (cKO) mice. (A) Representative images of coronal sections through the postnatal day 8 brain stained with 4,6‐diamidino‐2‐phenylindole (DAPI). Lines indicate measurements of cortex (ctx) thickness and corpus callosum (cc) thickness. (B) Both female and male cKO mice had reduced cortex thickness (one‐way analysis of variance [ANOVA] with Bonferroni post hoc comparisons, F 3,16 = 31.51, p < .0001; post hoc p < .001 in females and p < .0001 in males). (C) No differences in corpus callosum thickness were observed. (D–F) Representative images of coronal sections through the cortex stained with layer markers BRN2 (layers II/III), SATB2 (layers II–IV), and CTIP2 (layers V/VI). Cortex was divided into six equal bins from the ventricle to cortical surface to analyze distribution of positive immunofluorescent area. (G) BRN2 staining was more widely distributed in female and male cKO mice compared to floxed controls, with significantly decreased BRN2 positivity in bin 1 of both sexes and increased BRN2 staining found in bin 2 ( n = 3–4 per group, 2–3 sections per brain; two‐way ANOVA with Bonferroni post hoc comparisons; interaction of genotype × cortical layer, F 15,96 = 12.55, p < .0001; post hoc comparisons shown). (H) SATB2 staining was reduced in male cKO mice compared to floxed controls in bin 2 and bin 3 ( n = 3–4 per group, 2–3 sections per brain; two‐way ANOVA with Bonferroni post hoc comparisons; effect of genotype, F 3,90 = 3.618, p < .05; post hoc comparisons shown). (I) No significant differences were observed in CTIP2 staining across cortical bins. (J) <t>OLIG2</t> immunoreactivity was quantified in an region of interest containing the cortex–white matter junction (blue box). (K) OLIG2‐positive cell density was significantly increased in the cortex–white matter junction of male and female cKO mice compared to floxed controls ( n = 3–4 per group, 2–3 sections per brain; two‐tailed t ‐tests, p < .05). Data are shown as mean ± SEM. * p < .05, *** p < .001, **** p < .0001.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_7420/pmc11647420/pmc11647420__EPI-65-3717-g005.jpg)