rabbit anti qki5 Search Results


rabbit anti qki5  (Bethyl)
93
Bethyl rabbit anti qki5
Rabbit Anti Qki5, supplied by Bethyl, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti qki5/product/Bethyl
Average 93 stars, based on 1 article reviews
rabbit anti qki5 - by Bioz Stars, 2026-03
93/100 stars
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anti qki 5  (Bethyl)
92
Bethyl anti qki 5
(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an <t>anti–Qki-5</t> antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).
Anti Qki 5, supplied by Bethyl, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti qki 5/product/Bethyl
Average 92 stars, based on 1 article reviews
anti qki 5 - by Bioz Stars, 2026-03
92/100 stars
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anti–qki-5  (GenScript corporation)
90
GenScript corporation anti–qki-5
(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an <t>anti–Qki-5</t> antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).
Anti–Qki 5, supplied by GenScript corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti–qki-5/product/GenScript corporation
Average 90 stars, based on 1 article reviews
anti–qki-5 - by Bioz Stars, 2026-03
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qki-5  (Millipore)
90
Millipore qki-5
(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an <t>anti–Qki-5</t> antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).
Qki 5, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/qki-5/product/Millipore
Average 90 stars, based on 1 article reviews
qki-5 - by Bioz Stars, 2026-03
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rabbit qki-5  (Millipore)
90
Millipore rabbit qki-5
(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an <t>anti–Qki-5</t> antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).
Rabbit Qki 5, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit qki-5/product/Millipore
Average 90 stars, based on 1 article reviews
rabbit qki-5 - by Bioz Stars, 2026-03
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antibodies anti-srebp2  (Cayman Chemical)
90
Cayman Chemical antibodies anti-srebp2
(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an <t>anti–Qki-5</t> antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).
Antibodies Anti Srebp2, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/antibodies anti-srebp2/product/Cayman Chemical
Average 90 stars, based on 1 article reviews
antibodies anti-srebp2 - by Bioz Stars, 2026-03
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rabbit anti-qki-5  (Millipore)
90
Millipore rabbit anti-qki-5
(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an <t>anti–Qki-5</t> antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).
Rabbit Anti Qki 5, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti-qki-5/product/Millipore
Average 90 stars, based on 1 article reviews
rabbit anti-qki-5 - by Bioz Stars, 2026-03
90/100 stars
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rabbit α-qki-5  (Millipore)
90
Millipore rabbit α-qki-5
(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an <t>anti–Qki-5</t> antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).
Rabbit α Qki 5, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit α-qki-5/product/Millipore
Average 90 stars, based on 1 article reviews
rabbit α-qki-5 - by Bioz Stars, 2026-03
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primary antibodies anti-qki-5  (Boston Biochem)
90
Boston Biochem primary antibodies anti-qki-5
(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an <t>anti–Qki-5</t> antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).
Primary Antibodies Anti Qki 5, supplied by Boston Biochem, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/primary antibodies anti-qki-5/product/Boston Biochem
Average 90 stars, based on 1 article reviews
primary antibodies anti-qki-5 - by Bioz Stars, 2026-03
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anti-mbp  (Millipore)
90
Millipore anti-mbp
(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an <t>anti–Qki-5</t> antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).
Anti Mbp, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti-mbp/product/Millipore
Average 90 stars, based on 1 article reviews
anti-mbp - by Bioz Stars, 2026-03
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anti-prmt5  (Millipore)
90
Millipore anti-prmt5
<t>PRMT1,</t> CARM1, and PRMT5 expression in the developing mouse brain. Total brain lysates were obtained from P1, P4, P7, P11, P14, P21, and adult mice. The expression of PRMT1, CARM1, and PRMT5 was analyzed by immunoblotting. MBP isoforms, observed as the two classical major isoforms, were used as markers of myelination, and β-tubulin was used as a loading control. The asterisk denotes a nonspecific band. The molecular mass markers are shown in kDa on the left.
Anti Prmt5, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti-prmt5/product/Millipore
Average 90 stars, based on 1 article reviews
anti-prmt5 - by Bioz Stars, 2026-03
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antibodies anti qki 5  (Proteintech)
93
Proteintech antibodies anti qki 5
<t>PRMT1,</t> CARM1, and PRMT5 expression in the developing mouse brain. Total brain lysates were obtained from P1, P4, P7, P11, P14, P21, and adult mice. The expression of PRMT1, CARM1, and PRMT5 was analyzed by immunoblotting. MBP isoforms, observed as the two classical major isoforms, were used as markers of myelination, and β-tubulin was used as a loading control. The asterisk denotes a nonspecific band. The molecular mass markers are shown in kDa on the left.
Antibodies Anti Qki 5, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/antibodies anti qki 5/product/Proteintech
Average 93 stars, based on 1 article reviews
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Image Search Results


(A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).

Journal: The Journal of Clinical Investigation

Article Title: Mature myelin maintenance requires Qki to coactivate PPAR β -RXR α –mediated lipid metabolism

doi: 10.1172/JCI131800

Figure Lengend Snippet: (A) GSEA shows the PPAR signaling pathway signature in freshly isolated mouse oligodendrocytes. (B) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by the detection of homologs of PPAR and RXR via immunoblotting. (C) Co-IP using an anti–Qki-5 antibody in differentiated oligodendrocytes, followed by detection of PPARβ via immunoblotting. Qk-knockout (Qk-KO) cells served as a negative control to exclude nonspecific immunoprecipitation from the anti–Qki-5 antibody. (D) Reciprocal co-IP using an anti-PPARβ antibody, blotted with an anti–Qki-5 antibody. An IgG antibody served as a negative control. (E) Co-IP of Qki-5 and PPARβ in differentiated oligodendrocytes that were treated with RNase A while alive. (F) Co-IP of HA–Qki-5 (WT or V157E mutant) and PPARβ in differentiated oligodendrocytes. (G) Overlap of ChIP-seq peak sets of Qki-5, PPARβ, and HA in differentiated oligodendrocytes with ectopic expression of HA-PPARβ. (H) Genomic global distribution of the ChIP-seq peaks of Qki-5, PPARβ, and HA. (I) ChIP-seq density heatmaps of Qki-5, PPARβ, HA, and Pol II within ± 1 kb of the transcription start site (TSS). All peaks are rank ordered from high to low Qki-5 occupancy. (J) Average genome-wide occupancies of Qki-5, PPARβ, HA, and Pol II within ± 2.5 kb of the TSS. (K) Representative ChIP-seq binding peaks of Qki-5, PPARβ, HA, and Pol II on gene loci associated with fatty acid metabolism. Data are representative of 3 independent experiments (B–F).

Article Snippet: The following antibodies were used for staining, according to their manufacturer’s directions: anti-Olig2 (catalog AB9610), anti-Olig2 (catalog MABN50), anti-aspartoacylase (anti-ASPA) (catalog ABN1698), and anti-MBP (QD-9; catalog AB5864) were from Merck Millipore; anti-IBA1 (catalog ab107159), anti-Brdu (catalog ab6326), anti-PLP (catalog ab105784), anti-PPARβ (catalog ab137724), and anti-CD68 (catalog ab955) were from Abcam; anti-MAG (catalog 9043), anti-PDGFRα (catalog 3174), and anti–cleaved caspase 3 (catalog 9661) were from Cell Signaling Technology; anti-QKI (catalog SAB5201536) was from Sigma-Aldrich; anti-GFAP (catalog 556330) was from BD Biosciences; anti-GSTpi (catalog 311) was from MBL International; anti-MBP (catalog SMI-94R) was from Covance; anti–QKI-5 (catalog IHC-00574) was from Bethyl Laboratories; anti–QKI-6 (catalog 75-190) and anti-AnkG (catalog MABN466) were from NeuroMab; anti–QKI-7 was from a rabbit immunized with a short synthetic peptide (KGGPIEPSGVLEWIEMPVMPDISAH); anti-CD3 (catalog A0452) was from DAKO; and anti-Caspr was a gift from Matthew N. Rasband (Baylor College of Medicine, Houston, Texas, USA).

Techniques: Isolation, Co-Immunoprecipitation Assay, Western Blot, Knock-Out, Negative Control, Immunoprecipitation, Mutagenesis, ChIP-sequencing, Expressing, Genome Wide, Binding Assay

(A and B) Quantification of staining of FluoroMyelin (A) and PLP (B) in the frontal lobes from 5 human brains without neurological disease (control) and 30 lesions from 6 patients with PPMS. (C) Scatter plot of FluoroMyelin intensity versus PLP intensity in the samples in A. The solid lines among red dots represent the average levels of FluoroMyelin and PLP in controls. (D–H) Representative images (D) and quantification of FluoroMyelin level (E), PLP level (F), OLIG2+ cell number (G), and QKI-5 level (H) in controls and 3 subtypes of PPMS lesions, which were divided according to the level of FluoroMyelin and PLP in C. n = 5 in the control group; n = 3 in the FlhiPLPlo group; n = 15 in the FlloPLPhi group; n = 12 in the FlloPLPlo group. Scale bars: 50 μm. (I and J) Comparison of GSEA of fatty acid metabolism pathways (I) and the NES (J) between MS lesions and the controls. Box plots indicate medians, interquartile values, ranges, and individual pathways. BUFA, biosynthesis of unsaturated fatty acids; FAB, fatty acid biosynthesis; FAD, fatty acid degradation; FAE, fatty acid elongation; FAM, fatty acid metabolism; GM, glycerophospholipid metabolism; SM, sphingolipid metabolism. Data are mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 by Student’s t test (A and B), 1-way ANOVA followed by Bonferroni’s post hoc test (E–H), or Wilcoxon’s signed-rank test (J). NS, not significant.

Journal: The Journal of Clinical Investigation

Article Title: Mature myelin maintenance requires Qki to coactivate PPAR β -RXR α –mediated lipid metabolism

doi: 10.1172/JCI131800

Figure Lengend Snippet: (A and B) Quantification of staining of FluoroMyelin (A) and PLP (B) in the frontal lobes from 5 human brains without neurological disease (control) and 30 lesions from 6 patients with PPMS. (C) Scatter plot of FluoroMyelin intensity versus PLP intensity in the samples in A. The solid lines among red dots represent the average levels of FluoroMyelin and PLP in controls. (D–H) Representative images (D) and quantification of FluoroMyelin level (E), PLP level (F), OLIG2+ cell number (G), and QKI-5 level (H) in controls and 3 subtypes of PPMS lesions, which were divided according to the level of FluoroMyelin and PLP in C. n = 5 in the control group; n = 3 in the FlhiPLPlo group; n = 15 in the FlloPLPhi group; n = 12 in the FlloPLPlo group. Scale bars: 50 μm. (I and J) Comparison of GSEA of fatty acid metabolism pathways (I) and the NES (J) between MS lesions and the controls. Box plots indicate medians, interquartile values, ranges, and individual pathways. BUFA, biosynthesis of unsaturated fatty acids; FAB, fatty acid biosynthesis; FAD, fatty acid degradation; FAE, fatty acid elongation; FAM, fatty acid metabolism; GM, glycerophospholipid metabolism; SM, sphingolipid metabolism. Data are mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 by Student’s t test (A and B), 1-way ANOVA followed by Bonferroni’s post hoc test (E–H), or Wilcoxon’s signed-rank test (J). NS, not significant.

Article Snippet: The following antibodies were used for staining, according to their manufacturer’s directions: anti-Olig2 (catalog AB9610), anti-Olig2 (catalog MABN50), anti-aspartoacylase (anti-ASPA) (catalog ABN1698), and anti-MBP (QD-9; catalog AB5864) were from Merck Millipore; anti-IBA1 (catalog ab107159), anti-Brdu (catalog ab6326), anti-PLP (catalog ab105784), anti-PPARβ (catalog ab137724), and anti-CD68 (catalog ab955) were from Abcam; anti-MAG (catalog 9043), anti-PDGFRα (catalog 3174), and anti–cleaved caspase 3 (catalog 9661) were from Cell Signaling Technology; anti-QKI (catalog SAB5201536) was from Sigma-Aldrich; anti-GFAP (catalog 556330) was from BD Biosciences; anti-GSTpi (catalog 311) was from MBL International; anti-MBP (catalog SMI-94R) was from Covance; anti–QKI-5 (catalog IHC-00574) was from Bethyl Laboratories; anti–QKI-6 (catalog 75-190) and anti-AnkG (catalog MABN466) were from NeuroMab; anti–QKI-7 was from a rabbit immunized with a short synthetic peptide (KGGPIEPSGVLEWIEMPVMPDISAH); anti-CD3 (catalog A0452) was from DAKO; and anti-Caspr was a gift from Matthew N. Rasband (Baylor College of Medicine, Houston, Texas, USA).

Techniques: Staining

PRMT1, CARM1, and PRMT5 expression in the developing mouse brain. Total brain lysates were obtained from P1, P4, P7, P11, P14, P21, and adult mice. The expression of PRMT1, CARM1, and PRMT5 was analyzed by immunoblotting. MBP isoforms, observed as the two classical major isoforms, were used as markers of myelination, and β-tubulin was used as a loading control. The asterisk denotes a nonspecific band. The molecular mass markers are shown in kDa on the left.

Journal: The Journal of Biological Chemistry

Article Title: Type II Arginine Methyltransferase PRMT5 Regulates Gene Expression of Inhibitors of Differentiation/DNA Binding Id2 and Id4 during Glial Cell Differentiation *

doi: 10.1074/jbc.M111.277046

Figure Lengend Snippet: PRMT1, CARM1, and PRMT5 expression in the developing mouse brain. Total brain lysates were obtained from P1, P4, P7, P11, P14, P21, and adult mice. The expression of PRMT1, CARM1, and PRMT5 was analyzed by immunoblotting. MBP isoforms, observed as the two classical major isoforms, were used as markers of myelination, and β-tubulin was used as a loading control. The asterisk denotes a nonspecific band. The molecular mass markers are shown in kDa on the left.

Article Snippet: Anti-QKI-5 anti-QKI-6, anti-PRMT1, anti-PRMT5, and anti-MBP rabbit polyclonal antibodies were obtained from Millipore Inc. Anti-CARM1 antibody was from Active Motif Inc.

Techniques: Expressing, Western Blot