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Proteintech batf2
Batf2, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+batf2/pmc10535701__ijbsv19p4476s1-77-18-19?v=Proteintech
Average 93 stars, based on 5 article reviews

batf2 - by Bioz Stars, 2026-07

93/100 stars

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Loss of BATF2 increases expression of proliferative markers in astrocytes. A and B, wildtype ( A ) and Batf2 −/− ( B ) astrocytes labeled for H3Ser10ph, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. C and D, wildtype ( C ) and Batf2 −/− ( D ) astrocytes labeled for Ki67, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. E and F, wildtype ( E ) and Batf2 −/− ( F ) astrocytes labeled for pMCM2, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. G, quantification of H3Ser10ph-positive nuclei for wildtype and Batf2 −/− mice. Data were normalized to the total nuclei count, and data points are representative of individual mice. ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. H, quantification of colocalization between H3Ser10ph and DAPI. Data points are representative of individual mice. ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. I, quantification of Ki67-positive nuclei for wildtype and Batf2 −/− mice. Data points were normalized to the total nuclei count and are representative of individual mice. ∗∗∗∗ p < 0.0001 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. J, quantification of colocalization between Ki67 and DAPI. Data points are representative of individual mice. ∗∗∗ p < 0.001 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. K, quantification of pMCM2-positive nuclei for wildtype and Batf2 −/− mice. Data points were normalized to the total nuclei count and are representative of individual mice. ∗∗∗ p < 0.001 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. L, quantification of colocalization between pMCM2 and DAPI. Data points are representative of individual mice. ∗ p < 0.05 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. M, quantification of Ccnb1 transcript expression in wildtype and Batf2 −/− astrocytes. Data points were normalized to the wildtype average and are representative of individual mice. ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. N, representative Western blot of whole-cell cyclin B1 and vinculin protein levels of wildtype and Batf2 −/− astrocytes. O, quantification of whole-cell cyclin B1 protein levels in wildtype and Batf2 −/− astrocytes shown in N , normalized to vinculin expression. Data points are representative of individual mice. ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. P, cell viability assay of wildtype and Batf2 −/− astrocytes over 96 h. Data points are representative of the combined average of individual mouse absorbance values at 450 nm ( Batf2 +/+ N = 4, Batf2 −/− N = 4 per timepoint). ∗ p < 0.05 compared with wildtype samples by one-way ANOVA. The bars represent mean ± SEM. Q, live cell counts of wildtype and Batf2 −/− astrocytes over 96 h. Data points are representative of the combined average of individual mouse live cell counts ( Batf2 +/+ N = 4, Batf2 −/− N = 4 per timepoint). ∗ p < 0.05, ∗∗ p < 0.01 compared with wildtype samples by one-way ANOVA. The bars represent mean ± SEM. BATF2, basic leucine zipper ATF-like transcription factor 2; DAPI, 4′,6-diamidino-2-phenylindole; pMCM2, phospho-mini chromosome maintenance protein 2.

Journal: The Journal of Biological Chemistry

Article Title: BATF2-mediated control of astrocyte proliferation

doi: 10.1016/j.jbc.2025.110710

Figure Lengend Snippet: Loss of BATF2 increases expression of proliferative markers in astrocytes. A and B, wildtype ( A ) and Batf2 −/− ( B ) astrocytes labeled for H3Ser10ph, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. C and D, wildtype ( C ) and Batf2 −/− ( D ) astrocytes labeled for Ki67, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. E and F, wildtype ( E ) and Batf2 −/− ( F ) astrocytes labeled for pMCM2, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. G, quantification of H3Ser10ph-positive nuclei for wildtype and Batf2 −/− mice. Data were normalized to the total nuclei count, and data points are representative of individual mice. ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. H, quantification of colocalization between H3Ser10ph and DAPI. Data points are representative of individual mice. ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. I, quantification of Ki67-positive nuclei for wildtype and Batf2 −/− mice. Data points were normalized to the total nuclei count and are representative of individual mice. ∗∗∗∗ p < 0.0001 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. J, quantification of colocalization between Ki67 and DAPI. Data points are representative of individual mice. ∗∗∗ p < 0.001 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. K, quantification of pMCM2-positive nuclei for wildtype and Batf2 −/− mice. Data points were normalized to the total nuclei count and are representative of individual mice. ∗∗∗ p < 0.001 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. L, quantification of colocalization between pMCM2 and DAPI. Data points are representative of individual mice. ∗ p < 0.05 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. M, quantification of Ccnb1 transcript expression in wildtype and Batf2 −/− astrocytes. Data points were normalized to the wildtype average and are representative of individual mice. ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. N, representative Western blot of whole-cell cyclin B1 and vinculin protein levels of wildtype and Batf2 −/− astrocytes. O, quantification of whole-cell cyclin B1 protein levels in wildtype and Batf2 −/− astrocytes shown in N , normalized to vinculin expression. Data points are representative of individual mice. ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. P, cell viability assay of wildtype and Batf2 −/− astrocytes over 96 h. Data points are representative of the combined average of individual mouse absorbance values at 450 nm ( Batf2 +/+ N = 4, Batf2 −/− N = 4 per timepoint). ∗ p < 0.05 compared with wildtype samples by one-way ANOVA. The bars represent mean ± SEM. Q, live cell counts of wildtype and Batf2 −/− astrocytes over 96 h. Data points are representative of the combined average of individual mouse live cell counts ( Batf2 +/+ N = 4, Batf2 −/− N = 4 per timepoint). ∗ p < 0.05, ∗∗ p < 0.01 compared with wildtype samples by one-way ANOVA. The bars represent mean ± SEM. BATF2, basic leucine zipper ATF-like transcription factor 2; DAPI, 4′,6-diamidino-2-phenylindole; pMCM2, phospho-mini chromosome maintenance protein 2.

Article Snippet: Slides were blocked with 10% goat serum (Sigma) and 0.3% Triton X-100 for 15 min at room temperature and then incubated with primary antibodies for BATF2 (Santa Cruz; SC293274), cyclin D1 (Santa Cruz; SC717), phospho-histone H3 (Ser10) (Cell Signaling; 9701S), Ki67 (Abcam; AB15580), pMCM2 (Ser139) (D1Z8X) (Cell Signaling; 12958S), and CKS1B (Invitrogen; 36-6800) overnight at 4 °C.

Techniques: Expressing, Labeling, Two Tailed Test, Western Blot, Viability Assay

BATF2 binds to DNA motifs associated with cell cycle genes in astrocytes. A and B, IPA of top-regulated molecular functions ( A ) and diseases ( B ) by BATF2 in human astrocytes. C, adapted IPA S phase pathway. D, adapted IPA cell cycle regulation by BTG protein pathway. E–G, ChIP sequencing peak region counts of BATF2-binding events at the CKS1B ( E ) , CDK2 ( F ) , and CCND1 ( G ) gene loci and CpG islands in human astrocytes. BATF2, basic leucine zipper ATF-like transcription factor 2; ChIP, chromatin immunoprecipitation; IPA, ingenuity pathway analyses.

Journal: The Journal of Biological Chemistry

Article Title: BATF2-mediated control of astrocyte proliferation

doi: 10.1016/j.jbc.2025.110710

Figure Lengend Snippet: BATF2 binds to DNA motifs associated with cell cycle genes in astrocytes. A and B, IPA of top-regulated molecular functions ( A ) and diseases ( B ) by BATF2 in human astrocytes. C, adapted IPA S phase pathway. D, adapted IPA cell cycle regulation by BTG protein pathway. E–G, ChIP sequencing peak region counts of BATF2-binding events at the CKS1B ( E ) , CDK2 ( F ) , and CCND1 ( G ) gene loci and CpG islands in human astrocytes. BATF2, basic leucine zipper ATF-like transcription factor 2; ChIP, chromatin immunoprecipitation; IPA, ingenuity pathway analyses.

Techniques: ChIP-sequencing, Binding Assay, Chromatin Immunoprecipitation

BATF2 regulates cell cycle machinery expression in astrocytes. A–C, quantification of Cks1b ( A ), Cdk2 ( B ), and Ccnd1 ( C ) transcript expression in wildtype and Batf2 −/− astrocytes. Data points were normalized to the wildtype average and are representative of individual mice. ∗ p < 0.05, ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. D, representative Western blot of whole-cell cyclin D1 and vinculin protein levels in wildtype and Batf2 −/− astrocytes. E, quantification of whole-cell cyclin D1 protein levels in wildtype and Batf2 −/− astrocytes shown in D , normalized to vinculin expression. Data points are representative of individual mice. The bars represent mean ± SEM. F and G, wildtype ( F ) and Batf2 −/− ( G ) astrocytes labeled for cyclin D1, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. H and I, quantification of cyclin D1-positive area ( H ) and intensity ( I ) for wildtype and Batf2 −/− mice. Data points were normalized to actin expression and are representative of individual mice. ∗ p < 0.05 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. BATF2, basic leucine zipper ATF-like transcription factor 2; DAPI, 4′,6-diamidino-2-phenylindole.

Journal: The Journal of Biological Chemistry

Article Title: BATF2-mediated control of astrocyte proliferation

doi: 10.1016/j.jbc.2025.110710

Figure Lengend Snippet: BATF2 regulates cell cycle machinery expression in astrocytes. A–C, quantification of Cks1b ( A ), Cdk2 ( B ), and Ccnd1 ( C ) transcript expression in wildtype and Batf2 −/− astrocytes. Data points were normalized to the wildtype average and are representative of individual mice. ∗ p < 0.05, ∗∗ p < 0.01 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. D, representative Western blot of whole-cell cyclin D1 and vinculin protein levels in wildtype and Batf2 −/− astrocytes. E, quantification of whole-cell cyclin D1 protein levels in wildtype and Batf2 −/− astrocytes shown in D , normalized to vinculin expression. Data points are representative of individual mice. The bars represent mean ± SEM. F and G, wildtype ( F ) and Batf2 −/− ( G ) astrocytes labeled for cyclin D1, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. H and I, quantification of cyclin D1-positive area ( H ) and intensity ( I ) for wildtype and Batf2 −/− mice. Data points were normalized to actin expression and are representative of individual mice. ∗ p < 0.05 compared with wildtype samples by two-tailed Student's t test. The bars represent mean ± SEM. BATF2, basic leucine zipper ATF-like transcription factor 2; DAPI, 4′,6-diamidino-2-phenylindole.

Techniques: Expressing, Two Tailed Test, Western Blot, Labeling

Overexpression of BATF2 in U87-MG cells limits the expression of target cell cycle genes. A–D, quantification of BATF2 ( A ), CKS1B ( B ), CDK2 ( C ), and CCND1 ( D ) gene expression in human astrocytes and U87-MG cells. Data points were normalized to the human astrocyte average and are representative of replicates from two independent experiments. ∗ p < 0.05, ∗∗ p < 0.01 compared with human astrocyte samples by two-tailed Student's t test. The bars represent mean ± SEM. E and F, human astrocytes ( E ) and U87-MG cells ( F ) labeled for BATF2, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. G and H, quantification of BATF2-positive area ( G ) and intensity ( H ) for human astrocytes and U87-MG cells. Data points were normalized to actin expression and are representative of replicates from two independent experiments. ∗ p < 0.05 compared with human astrocyte samples by two-tailed Student's t test. The bars represent mean ± SEM. I, representative Western blot of whole-cell BATF2, cyclin D1, and vinculin protein levels in human astrocytes and U87-MG cells. J–K, quantification of whole-cell BATF2 ( J ) and cyclin D1 ( K ) protein levels of human astrocytes and U87-MG cells shown in I , normalized to vinculin expression. Data points are representative of replicates from two independent experiments. The bars represent mean ± SEM. BATF2, basic leucine zipper ATF-like transcription factor 2; DAPI, 4′,6-diamidino-2-phenylindole.

Journal: The Journal of Biological Chemistry

Article Title: BATF2-mediated control of astrocyte proliferation

doi: 10.1016/j.jbc.2025.110710

Figure Lengend Snippet: Overexpression of BATF2 in U87-MG cells limits the expression of target cell cycle genes. A–D, quantification of BATF2 ( A ), CKS1B ( B ), CDK2 ( C ), and CCND1 ( D ) gene expression in human astrocytes and U87-MG cells. Data points were normalized to the human astrocyte average and are representative of replicates from two independent experiments. ∗ p < 0.05, ∗∗ p < 0.01 compared with human astrocyte samples by two-tailed Student's t test. The bars represent mean ± SEM. E and F, human astrocytes ( E ) and U87-MG cells ( F ) labeled for BATF2, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. G and H, quantification of BATF2-positive area ( G ) and intensity ( H ) for human astrocytes and U87-MG cells. Data points were normalized to actin expression and are representative of replicates from two independent experiments. ∗ p < 0.05 compared with human astrocyte samples by two-tailed Student's t test. The bars represent mean ± SEM. I, representative Western blot of whole-cell BATF2, cyclin D1, and vinculin protein levels in human astrocytes and U87-MG cells. J–K, quantification of whole-cell BATF2 ( J ) and cyclin D1 ( K ) protein levels of human astrocytes and U87-MG cells shown in I , normalized to vinculin expression. Data points are representative of replicates from two independent experiments. The bars represent mean ± SEM. BATF2, basic leucine zipper ATF-like transcription factor 2; DAPI, 4′,6-diamidino-2-phenylindole.

Techniques: Over Expression, Expressing, Gene Expression, Two Tailed Test, Labeling, Western Blot

Knockdown of BATF2 upregulates cell cycle genes in U87-MG cells. A–D, quantification of BATF2 ( A ), CKS1B ( B ), CDK2 ( C ), and CCND1 ( D ) gene expression in U87-MG cells treated with siControl or si BATF2 for 72 h. Data points were normalized to the siControl average and are representative of replicates from two independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. E–G, U87-MG cells treated with siControl ( E ) and si BATF2 ( F and G ) labeled for BATF2, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. H and I, quantification of BATF2-positive area ( H ) and intensity ( I ) for U87-MG cells treated with siControl or si BATF2 . Data points were normalized to actin expression and are representative of technical replicates. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. J–L, U87-MG cells treated with siControl ( J ) and si BATF2 ( K and L) labeled for cyclin D1, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. M and N, quantification of cyclin D1-positive area ( M ) and intensity ( N ) for U87-MG cells treated with siControl or si BATF2 . Data points were normalized to actin expression and are representative of technical replicates. ∗ p < 0.05, ∗∗ p < 0.01 compared with siControl samples by one-way ANOVA. O–Q, U87-MG cells treated with siControl ( O ) and si BATF2 ( P and Q ) labeled for Ki67, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. R and S, quantification of Ki67-positive nuclei for siControl or si BATF2 -treated U87-MG cells. Data points in R were normalized to the total nuclei count. Data shown in R and S are representative of technical replicates. ∗ p < 0.05 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. T, quantification of CCNB1 transcript expression in siControl or si BATF2 -treated U87-MG cells. Data points were normalized to the siControl average and are representative of replicates from two independent experiments. ∗∗∗∗ p < 0.0001 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. U, cell viability assay of siControl or si BATF2- treated U87-MG cells over 96 h. Data points are representative of the combined average of absorbance values at 450 nm from individual replicates from two independent experiments (siControl N = 4–6, si BATF2 (149104) N = 5–6, si BATF2 (36727) N = 4 to 6 per timepoint). ∗∗ p < 0.01 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. V, live cell counts for siControl or si BATF2 -treated U87-MG cells over 96 h. Data points are representative of the combined average of live cell counts of individual replicates from two independent experiments. (siControl N = 4, si BATF2 (149104) N = 3–4, si BATF2 (36727) N = 4 per timepoint). ∗∗∗ p < 0.001 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. BATF2, basic leucine zipper ATF-like transcription factor 2; DAPI, 4′,6-diamidino-2-phenylindole.

Journal: The Journal of Biological Chemistry

Article Title: BATF2-mediated control of astrocyte proliferation

doi: 10.1016/j.jbc.2025.110710

Figure Lengend Snippet: Knockdown of BATF2 upregulates cell cycle genes in U87-MG cells. A–D, quantification of BATF2 ( A ), CKS1B ( B ), CDK2 ( C ), and CCND1 ( D ) gene expression in U87-MG cells treated with siControl or si BATF2 for 72 h. Data points were normalized to the siControl average and are representative of replicates from two independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. E–G, U87-MG cells treated with siControl ( E ) and si BATF2 ( F and G ) labeled for BATF2, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. H and I, quantification of BATF2-positive area ( H ) and intensity ( I ) for U87-MG cells treated with siControl or si BATF2 . Data points were normalized to actin expression and are representative of technical replicates. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. J–L, U87-MG cells treated with siControl ( J ) and si BATF2 ( K and L) labeled for cyclin D1, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. M and N, quantification of cyclin D1-positive area ( M ) and intensity ( N ) for U87-MG cells treated with siControl or si BATF2 . Data points were normalized to actin expression and are representative of technical replicates. ∗ p < 0.05, ∗∗ p < 0.01 compared with siControl samples by one-way ANOVA. O–Q, U87-MG cells treated with siControl ( O ) and si BATF2 ( P and Q ) labeled for Ki67, actin, and nuclei counterstained with DAPI. The scale bars represent 50 μm. R and S, quantification of Ki67-positive nuclei for siControl or si BATF2 -treated U87-MG cells. Data points in R were normalized to the total nuclei count. Data shown in R and S are representative of technical replicates. ∗ p < 0.05 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. T, quantification of CCNB1 transcript expression in siControl or si BATF2 -treated U87-MG cells. Data points were normalized to the siControl average and are representative of replicates from two independent experiments. ∗∗∗∗ p < 0.0001 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. U, cell viability assay of siControl or si BATF2- treated U87-MG cells over 96 h. Data points are representative of the combined average of absorbance values at 450 nm from individual replicates from two independent experiments (siControl N = 4–6, si BATF2 (149104) N = 5–6, si BATF2 (36727) N = 4 to 6 per timepoint). ∗∗ p < 0.01 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. V, live cell counts for siControl or si BATF2 -treated U87-MG cells over 96 h. Data points are representative of the combined average of live cell counts of individual replicates from two independent experiments. (siControl N = 4, si BATF2 (149104) N = 3–4, si BATF2 (36727) N = 4 per timepoint). ∗∗∗ p < 0.001 compared with siControl samples by one-way ANOVA. The bars represent mean ± SEM. BATF2, basic leucine zipper ATF-like transcription factor 2; DAPI, 4′,6-diamidino-2-phenylindole.

Techniques: Knockdown, Gene Expression, Labeling, Expressing, Viability Assay

BATF2 expression negatively correlates with cyclin D1 levels in GBM. A, overall survival outcomes relative to BATF2 expression in GBM patients. B, quantification of BATF2 expression between GBM and nontumor samples (GBM N = 163, nontumor N = 207). Data represented in A and B were obtained from TCGA and GTEx publicly available data sets and were analyzed using Gepia2. ∗ p < 0.05 compared with nontumor samples. The bars represent mean ± SD. C and D, quantification of BATF2 ( C ) and CCND1 ( D ) gene expression in human astrocytes and GBM patient samples. Data points were normalized to the human astrocyte average. Human astrocyte data points are representative of technical replicates. GBM data points are representative of individual patients. The bars represent mean ± SEM. E, regression analysis of CCND1 versus BATF2 gene expression in GBM patients. Data points were analyzed by simple linear regression and are representative of individual patients. F, representative Western blot of whole-cell BATF2, cyclin D1, and beta-actin protein levels in human astrocytes and GBM patient samples. G, regression analysis of cyclin D1 versus BATF2 protein expression in GBM patients. Data points were analyzed by simple linear regression and are representative of individual patients. BATF2, basic leucine zipper ATF-like transcription factor 2; GBM, glioblastoma multiforme; GTEx, Genotype-Tissue Expression; TCGA, The Cancer Genome Atlas.

Journal: The Journal of Biological Chemistry

Article Title: BATF2-mediated control of astrocyte proliferation

doi: 10.1016/j.jbc.2025.110710

Figure Lengend Snippet: BATF2 expression negatively correlates with cyclin D1 levels in GBM. A, overall survival outcomes relative to BATF2 expression in GBM patients. B, quantification of BATF2 expression between GBM and nontumor samples (GBM N = 163, nontumor N = 207). Data represented in A and B were obtained from TCGA and GTEx publicly available data sets and were analyzed using Gepia2. ∗ p < 0.05 compared with nontumor samples. The bars represent mean ± SD. C and D, quantification of BATF2 ( C ) and CCND1 ( D ) gene expression in human astrocytes and GBM patient samples. Data points were normalized to the human astrocyte average. Human astrocyte data points are representative of technical replicates. GBM data points are representative of individual patients. The bars represent mean ± SEM. E, regression analysis of CCND1 versus BATF2 gene expression in GBM patients. Data points were analyzed by simple linear regression and are representative of individual patients. F, representative Western blot of whole-cell BATF2, cyclin D1, and beta-actin protein levels in human astrocytes and GBM patient samples. G, regression analysis of cyclin D1 versus BATF2 protein expression in GBM patients. Data points were analyzed by simple linear regression and are representative of individual patients. BATF2, basic leucine zipper ATF-like transcription factor 2; GBM, glioblastoma multiforme; GTEx, Genotype-Tissue Expression; TCGA, The Cancer Genome Atlas.

Techniques: Expressing, Gene Expression, Western Blot

(A) PCA of RNA sequencing demonstrating distinct gene expression patterns of human spinal cord astrocytes treated with 10 ng/mL IFNγ, TNF-α, IL-1β, IL-17, GM-CSF, and media for 24 h. (B) Heatmap of top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent log2 fold change compared to media from 3 independent samples. (C) Top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent the log2 fold change compared to media from 3 independent samples. (D) BATF2 transcript levels of human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 0–48 h. ** p < 0.01 and *** p < 0.001 compared to media-treated samples by one-way ANOVA. Data points represent mean ± SEM ( n = 3). (E) BATF2 transcript levels of human spinal cord astrocytes treated with 10 ng/mL of various inflammatory stimuli for 24 h. **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n = 4). (F) Representative western blot of whole-cell BATF2 protein levels in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h. (G) Quantification of whole-cell BATF2 protein levels in primary human spinal cord astrocytes shown in (F), normalized to β-actin expression. * p < 0.05 compared to media-treated samples by one-way ANOVA. Bars represent mean ± SEM ( n = 3).

Journal: Cell reports

Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

doi: 10.1016/j.celrep.2025.115393

Figure Lengend Snippet: (A) PCA of RNA sequencing demonstrating distinct gene expression patterns of human spinal cord astrocytes treated with 10 ng/mL IFNγ, TNF-α, IL-1β, IL-17, GM-CSF, and media for 24 h. (B) Heatmap of top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent log2 fold change compared to media from 3 independent samples. (C) Top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent the log2 fold change compared to media from 3 independent samples. (D) BATF2 transcript levels of human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 0–48 h. ** p < 0.01 and *** p < 0.001 compared to media-treated samples by one-way ANOVA. Data points represent mean ± SEM ( n = 3). (E) BATF2 transcript levels of human spinal cord astrocytes treated with 10 ng/mL of various inflammatory stimuli for 24 h. **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n = 4). (F) Representative western blot of whole-cell BATF2 protein levels in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h. (G) Quantification of whole-cell BATF2 protein levels in primary human spinal cord astrocytes shown in (F), normalized to β-actin expression. * p < 0.05 compared to media-treated samples by one-way ANOVA. Bars represent mean ± SEM ( n = 3).

Article Snippet: Demyelinated lesions were identified and characterized using immunostaining for MBP (Abcam) and IBA1 (Wako) as previously described., Subsequent sections were exposed to antibodies specific for human BATF2 (Santa Cruz), IRF1 (Proteintech), Sox9 (R&D Systems), ALDH1L1 (Cell Signaling), and/or IBA1 (SPICA Dye 594-conjugated; Wako) for 4–5 days at 4°C.

Techniques: RNA Sequencing, Gene Expression, Western Blot, Expressing

(A) Merged peak region heatmap of BATF2 binding in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. Scale bar indicates BATF2 binding events per merged region. (B) Peak tag numbers of BATF2 binding events in 1,289 merged peak regions of human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. (C) Peak location of BATF2 binding events in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. hg38 binding events were used as an internal control. Data are the average peak locations between two independent samples per treatment. (D and E) Top BATF2 binding motifs of media- and IFNγ-treated human spinal cord astrocytes. Data shown in (A)–(E) are representative of two independent samples per treatment.

Journal: Cell reports

Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

doi: 10.1016/j.celrep.2025.115393

Figure Lengend Snippet: (A) Merged peak region heatmap of BATF2 binding in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. Scale bar indicates BATF2 binding events per merged region. (B) Peak tag numbers of BATF2 binding events in 1,289 merged peak regions of human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. (C) Peak location of BATF2 binding events in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. hg38 binding events were used as an internal control. Data are the average peak locations between two independent samples per treatment. (D and E) Top BATF2 binding motifs of media- and IFNγ-treated human spinal cord astrocytes. Data shown in (A)–(E) are representative of two independent samples per treatment.

Techniques: Binding Assay, Control

(A) Ingenuity pathway analysis of top regulated pathways by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (B) Graphical summary of predicated targets regulated by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (C) Adapted ingenuity pathway analysis: IFNγ signaling pathway from (A). (D) Adapted ingenuity pathway analysis: multiple sclerosis signaling pathway from (A). (E) Peak region counts of BATF2 binding events upstream of the IRF1 gene locus and at CpG islands in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h (green) or media (gray). (F–K) Quantification of Irf1 and target gene transcript expression in Batf2 +/+ and Batf2 −/− primary murine spinal cord astrocytes stimulated with media or 10 ng/mL IFNγ for 48 h. Data are representative of 2 independent experiments. Individual data points were normalized to the media average and are representative of individual mice. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n =7). Data shown in (A)–(E) are representative of two independent samples per treatment.

Journal: Cell reports

Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

doi: 10.1016/j.celrep.2025.115393

Figure Lengend Snippet: (A) Ingenuity pathway analysis of top regulated pathways by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (B) Graphical summary of predicated targets regulated by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (C) Adapted ingenuity pathway analysis: IFNγ signaling pathway from (A). (D) Adapted ingenuity pathway analysis: multiple sclerosis signaling pathway from (A). (E) Peak region counts of BATF2 binding events upstream of the IRF1 gene locus and at CpG islands in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h (green) or media (gray). (F–K) Quantification of Irf1 and target gene transcript expression in Batf2 +/+ and Batf2 −/− primary murine spinal cord astrocytes stimulated with media or 10 ng/mL IFNγ for 48 h. Data are representative of 2 independent experiments. Individual data points were normalized to the media average and are representative of individual mice. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n =7). Data shown in (A)–(E) are representative of two independent samples per treatment.

Techniques: Binding Assay, Expressing

(A and B) EAE was induced in Batf2 −/− and control mice. EAE (A) clinical course and (B) weights were blindly monitored. Data are a combination of 3 independent experiments and were analyzed using the Mann–Whitney U test for nonparametric data. ** p < 0.01 from day 2 and **** p < 0.0001. Data points represent mean ± SEM ( n = 8 per genotype). 25 days post-immunization, mice were sacrificed, and the CNS tissue was cryopreserved for immunofluorescent analysis. Ventral white matter tracts of the lumbar spinal cord were imaged using confocal microscopy. (C and D) Spinal cord tissue from (C) Batf2 +/+ and (D) Batf2 −/− mice labeled for MBP and nuclei counterstained with DAPI. Scale bars, 20 μm. (E) Quantification of MBP area normalized to the average of Batf2 +/+ control mice. ** p < 0.01 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (F and G) Spinal cord tissue from (F) Batf2 +/+ and (G) Batf2 −/− mice labeled for CD45 and nuclei counterstained with DAPI. Scale bars, 20 μm. (H and I) Quantification of CD45 area and lesion area normalized to the average of Batf2 +/+ control mice. ** p < 0.01 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (J and K) Spinal cord tissue from (J) Batf2 +/+ and (K) Batf2 −/− mice labeled for IRF1, SOX9, and nuclei counterstained with DAPI. Scale bars, 20 μm. (L–N) Quantification of IRF1 area normalized to the average of Batf2 +/+ control mice and IRF1 area in SOX9 + and SOX9 − cells normalized to lesion area and the average of Batf2 +/+ mice. * p < 0.05 and ** p < 0.01 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (O) Colocalization of SOX9 with IRF1 for Batf2 +/+ and Batf2 −/− mice. ** p < 0.01 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (P and Q) Spinal cord tissue from (N) Batf2 +/+ and (O) Batf2 −/− mice labeled for caspase-1, GFAP, and nuclei counterstained with DAPI. Scale bars, 20 μm. (R–T) Quantification of caspase-1 area normalized to the average of Batf2 +/+ control mice and caspase-1 area in GFAP + and GFAP − cells normalized to lesion area and the average of Batf2 +/+ mice. * p < 0.05 and *** p < 0.001 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (U) Colocalization of GFAP with caspase-1 for Batf2 +/+ and Batf2 −/− mice. *** p < 0.001 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. Data in (C)–(U) are representative of 3 independent experiments and include mice that survived until endpoint at day 25 ( n = 8 for Batf2 +/+ , n = 7 for Batf2 −/− ). Each data point is representative of an individual mouse.

Journal: Cell reports

Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

doi: 10.1016/j.celrep.2025.115393

Figure Lengend Snippet: (A and B) EAE was induced in Batf2 −/− and control mice. EAE (A) clinical course and (B) weights were blindly monitored. Data are a combination of 3 independent experiments and were analyzed using the Mann–Whitney U test for nonparametric data. ** p < 0.01 from day 2 and **** p < 0.0001. Data points represent mean ± SEM ( n = 8 per genotype). 25 days post-immunization, mice were sacrificed, and the CNS tissue was cryopreserved for immunofluorescent analysis. Ventral white matter tracts of the lumbar spinal cord were imaged using confocal microscopy. (C and D) Spinal cord tissue from (C) Batf2 +/+ and (D) Batf2 −/− mice labeled for MBP and nuclei counterstained with DAPI. Scale bars, 20 μm. (E) Quantification of MBP area normalized to the average of Batf2 +/+ control mice. ** p < 0.01 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (F and G) Spinal cord tissue from (F) Batf2 +/+ and (G) Batf2 −/− mice labeled for CD45 and nuclei counterstained with DAPI. Scale bars, 20 μm. (H and I) Quantification of CD45 area and lesion area normalized to the average of Batf2 +/+ control mice. ** p < 0.01 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (J and K) Spinal cord tissue from (J) Batf2 +/+ and (K) Batf2 −/− mice labeled for IRF1, SOX9, and nuclei counterstained with DAPI. Scale bars, 20 μm. (L–N) Quantification of IRF1 area normalized to the average of Batf2 +/+ control mice and IRF1 area in SOX9 + and SOX9 − cells normalized to lesion area and the average of Batf2 +/+ mice. * p < 0.05 and ** p < 0.01 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (O) Colocalization of SOX9 with IRF1 for Batf2 +/+ and Batf2 −/− mice. ** p < 0.01 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (P and Q) Spinal cord tissue from (N) Batf2 +/+ and (O) Batf2 −/− mice labeled for caspase-1, GFAP, and nuclei counterstained with DAPI. Scale bars, 20 μm. (R–T) Quantification of caspase-1 area normalized to the average of Batf2 +/+ control mice and caspase-1 area in GFAP + and GFAP − cells normalized to lesion area and the average of Batf2 +/+ mice. * p < 0.05 and *** p < 0.001 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. (U) Colocalization of GFAP with caspase-1 for Batf2 +/+ and Batf2 −/− mice. *** p < 0.001 compared to Batf2 +/+ samples by two-tailed Student’s t test. Bars represent mean ± SEM. Data in (C)–(U) are representative of 3 independent experiments and include mice that survived until endpoint at day 25 ( n = 8 for Batf2 +/+ , n = 7 for Batf2 −/− ). Each data point is representative of an individual mouse.

Techniques: Control, MANN-WHITNEY, Confocal Microscopy, Labeling, Two Tailed Test

(A) Human postmortem MS brain sections labeled for MBP and IBA1 to identify NAWM and chronic active lesions. Dotted line indicates the border of the LR and LC. Scale bars, 50 μm. (B) Chronic active lesion labeled for BATF2 and IBA1. Dotted line indicates the border of the LR and LC. Scale bars, 50 μm. (C) Quantification of BATF2 area. * p < 0.05 and ** p < 0.01 by two-tailed Student’s t test for each set of bars. Bars represent mean ± SEM. (D) Chronic active lesion labeled for IRF1 and IBA1. Dotted line indicates the border of the LR and LC. Scale bars, 50μm. (E) Quantification of IRF1 area. * p < 0.05 by two-tailed Student’s t test for each set of bars. Bars represent mean ± SEM. (F) Chronic active lesions labeled for BATF2 and SOX9 (top) and IRF1 and SOX9 (bottom). Dotted line indicates the border of the LR and LC. Scale bar, 50 μm. Green box indicates the area of interest within the LC. (Fi) High-magnification image of LC area of interest from (F) labeled for BATF2, IRF1, and SOX9. Scale bar, 10 μm. (Fii) Three-dimensional (3D) render of the high-magnification image from (Fi) labeled for BATF2, IRF1, and SOX9. Scale bar, 10 μm. (G) Quantification of colocalization between SOX9 and IBA1 with BATF2 (green) and IRF1 (blue). * p < 0.05 and ** p < 0.01 by one-way ANOVA for each set of bars. Bars represent mean ± SEM. (H) Quantification of colocalization of BATF2 and IRF1 in the LR and LC. Data were analyzed by a two-tailed Student’s t test. Bars represent mean ± SEM. Data in (C), (E), (G), and (H) are representative of 2 independent experiments and include all patients represented in ( n = 6). Each data point is representative of an individual patient. LR, lesion rim; LC, lesion core.

Journal: Cell reports

Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

doi: 10.1016/j.celrep.2025.115393

Figure Lengend Snippet: (A) Human postmortem MS brain sections labeled for MBP and IBA1 to identify NAWM and chronic active lesions. Dotted line indicates the border of the LR and LC. Scale bars, 50 μm. (B) Chronic active lesion labeled for BATF2 and IBA1. Dotted line indicates the border of the LR and LC. Scale bars, 50 μm. (C) Quantification of BATF2 area. * p < 0.05 and ** p < 0.01 by two-tailed Student’s t test for each set of bars. Bars represent mean ± SEM. (D) Chronic active lesion labeled for IRF1 and IBA1. Dotted line indicates the border of the LR and LC. Scale bars, 50μm. (E) Quantification of IRF1 area. * p < 0.05 by two-tailed Student’s t test for each set of bars. Bars represent mean ± SEM. (F) Chronic active lesions labeled for BATF2 and SOX9 (top) and IRF1 and SOX9 (bottom). Dotted line indicates the border of the LR and LC. Scale bar, 50 μm. Green box indicates the area of interest within the LC. (Fi) High-magnification image of LC area of interest from (F) labeled for BATF2, IRF1, and SOX9. Scale bar, 10 μm. (Fii) Three-dimensional (3D) render of the high-magnification image from (Fi) labeled for BATF2, IRF1, and SOX9. Scale bar, 10 μm. (G) Quantification of colocalization between SOX9 and IBA1 with BATF2 (green) and IRF1 (blue). * p < 0.05 and ** p < 0.01 by one-way ANOVA for each set of bars. Bars represent mean ± SEM. (H) Quantification of colocalization of BATF2 and IRF1 in the LR and LC. Data were analyzed by a two-tailed Student’s t test. Bars represent mean ± SEM. Data in (C), (E), (G), and (H) are representative of 2 independent experiments and include all patients represented in ( n = 6). Each data point is representative of an individual patient. LR, lesion rim; LC, lesion core.

Techniques: Labeling, Two Tailed Test

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