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Proteintech anti nr2f1
Anti Nr2f1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 15 article reviews

anti nr2f1 - by Bioz Stars, 2026-06

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The protein level of NR2F1 is increased in the ASC model. (A) The anesthetized and dilated mice were positioned beneath a microscope for the ASC modeling procedure. (B) Cataract lesions in control and ASC mice using a slit lamp. (C) Hematoxylin and eosin staining in lens section of control and ASC mice. Scale bar, 100 μm. (D) Masson staining of the two groups. Scale bar, 100 μm. (E) The immunofluorescence results of FN1 and VIM in lens slides of control and ASC groups. Scale bar, 50 μm. (F, G) The protein expression and quantification of apoptosis-related markers BAX and CASP3 in control and ASC groups. n = 3 per group; mean ± standard deviation; ∗∗ p < 0.01; unpaired student's t -test. (H, I) The protein level and quantitative chart of NR2F1 in the two groups mentioned above. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test. NR2F1, nuclear receptor subfamily 2 group F member 1; ASC, anterior subcapsular cataract; FN1, fibronectin 1; VIM, vimentin; BAX, Bcl-2-associated X; CASP3, caspase 3.

Journal: Genes & Diseases

Article Title: Autophagy-induced NR2F1 activation promotes the apoptosis of lens epithelial cells and facilitates cataract-associated fibrosis through targeting STAT3

doi: 10.1016/j.gendis.2025.101549

Figure Lengend Snippet: The protein level of NR2F1 is increased in the ASC model. (A) The anesthetized and dilated mice were positioned beneath a microscope for the ASC modeling procedure. (B) Cataract lesions in control and ASC mice using a slit lamp. (C) Hematoxylin and eosin staining in lens section of control and ASC mice. Scale bar, 100 μm. (D) Masson staining of the two groups. Scale bar, 100 μm. (E) The immunofluorescence results of FN1 and VIM in lens slides of control and ASC groups. Scale bar, 50 μm. (F, G) The protein expression and quantification of apoptosis-related markers BAX and CASP3 in control and ASC groups. n = 3 per group; mean ± standard deviation; ∗∗ p < 0.01; unpaired student's t -test. (H, I) The protein level and quantitative chart of NR2F1 in the two groups mentioned above. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test. NR2F1, nuclear receptor subfamily 2 group F member 1; ASC, anterior subcapsular cataract; FN1, fibronectin 1; VIM, vimentin; BAX, Bcl-2-associated X; CASP3, caspase 3.

Article Snippet: NR2F1 agonist 1 (HY-149913, MCE) was treated at 0.5 or 1 μM concentration.

Techniques: Microscopy, Control, Staining, Immunofluorescence, Expressing, Standard Deviation

Journal: Genes & Diseases

Article Title: Autophagy-induced NR2F1 activation promotes the apoptosis of lens epithelial cells and facilitates cataract-associated fibrosis through targeting STAT3

doi: 10.1016/j.gendis.2025.101549

Figure Lengend Snippet: TGF-β1 mediated autophagy dysfunction resulting in an increased protein level of NR2F1. (A) The mRNA profile of NR2F1 in lens epithelial cells and fiber cells using single-cell data. (B) The mRNA level of NR2F1 in SRA01/04 cells with PBS or TGF-β1. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test. (C, D) The protein expression and quantification of NR2F1 in TGF-β1-induced SRA01/04 cells. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test. (E) Subcellular location of NR2F1 in PBS- or TGF-β1-treated SRA01/04 cells. Scale bar, 50 μm. (F, G) The protein level and quantification of NR2F1 in SRA01/04 cells stimulated with the autophagy inhibitor chloroquine at concentrations of 5, 10, 20, 40, and 80 μM, respectively. n = 3 per group; mean ± standard deviation; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; one-way ANOVA. (H) Co-localization of LC3B and NR2F1 along with P62 and NR2F1 in SRA01/04 cells with TGF-β1. Scale bar, 50 μm. TGF-β1, transforming growth factor-β1; NR2F1, nuclear receptor subfamily 2 group F member 1; PBS, phosphate-buffered saline; LC3B, microtubule-associated protein 1 light-chain 3B.

Article Snippet: NR2F1 agonist 1 (HY-149913, MCE) was treated at 0.5 or 1 μM concentration.

Techniques: Standard Deviation, Expressing, Saline

Knockdown of NR2F1 significantly attenuates fibrosis both in vivo and in vitro . (A) Adeno-associated adenovirus (AAV) was administered into the anterior chamber of mouse eyes. (B) Representative pictures of the ASC modeling group versus the negative control group under a slit lamp following AAV injection. (C) Hematoxylin and eosin staining in the two groups mentioned above. Scale bar, 100 μm. (D) Masson staining in the two groups. Scale bar, 100 μm. (E) The immunofluorescence intensity of α-SMA in the lens sections of AAV-NC and AAV-NR2F1 ASC mice. Scale bar, 50 μm. (F, G) The protein level and quantification of NR2F1 in SRA01/04 cells transfected with Sh-NC, Sh-NR2F1-1, Sh-NR2F1-2, or Sh-NR2F1-3 lentivirus. n = 3 per group; mean ± standard deviation; ∗∗∗ p < 0.001; one-way ANOVA. (H–K) The protein expression and quantitative graphs of FN1, VIM, and α-SMA in TGF-β1-induced SRA01/04 cells with Sh-NC or Sh-NR2F1. n = 3 per group; mean ± standard deviation; ∗ p < 0.05, ∗∗ p < 0.01; unpaired student's t -test. (L – N) Immunofluorescence images of FN1, VIM, and α-SMA in TGF-β1-mediated SRA01/04 cells with Sh-NC or Sh-NR2F1. Scale bar, 100 μm. NR2F1, nuclear receptor subfamily 2 group F member 1; ASC, anterior subcapsular cataract; FN1, fibronectin 1; α-SMA, α-smooth muscle actin; VIM, vimentin; TGF-β1, transforming growth factor-β1.

Journal: Genes & Diseases

Article Title: Autophagy-induced NR2F1 activation promotes the apoptosis of lens epithelial cells and facilitates cataract-associated fibrosis through targeting STAT3

doi: 10.1016/j.gendis.2025.101549

Figure Lengend Snippet: Knockdown of NR2F1 significantly attenuates fibrosis both in vivo and in vitro . (A) Adeno-associated adenovirus (AAV) was administered into the anterior chamber of mouse eyes. (B) Representative pictures of the ASC modeling group versus the negative control group under a slit lamp following AAV injection. (C) Hematoxylin and eosin staining in the two groups mentioned above. Scale bar, 100 μm. (D) Masson staining in the two groups. Scale bar, 100 μm. (E) The immunofluorescence intensity of α-SMA in the lens sections of AAV-NC and AAV-NR2F1 ASC mice. Scale bar, 50 μm. (F, G) The protein level and quantification of NR2F1 in SRA01/04 cells transfected with Sh-NC, Sh-NR2F1-1, Sh-NR2F1-2, or Sh-NR2F1-3 lentivirus. n = 3 per group; mean ± standard deviation; ∗∗∗ p < 0.001; one-way ANOVA. (H–K) The protein expression and quantitative graphs of FN1, VIM, and α-SMA in TGF-β1-induced SRA01/04 cells with Sh-NC or Sh-NR2F1. n = 3 per group; mean ± standard deviation; ∗ p < 0.05, ∗∗ p < 0.01; unpaired student's t -test. (L – N) Immunofluorescence images of FN1, VIM, and α-SMA in TGF-β1-mediated SRA01/04 cells with Sh-NC or Sh-NR2F1. Scale bar, 100 μm. NR2F1, nuclear receptor subfamily 2 group F member 1; ASC, anterior subcapsular cataract; FN1, fibronectin 1; α-SMA, α-smooth muscle actin; VIM, vimentin; TGF-β1, transforming growth factor-β1.

Article Snippet: NR2F1 agonist 1 (HY-149913, MCE) was treated at 0.5 or 1 μM concentration.

Techniques: Knockdown, In Vivo, In Vitro, Negative Control, Injection, Staining, Immunofluorescence, Transfection, Standard Deviation, Expressing

NR2F1 inhibition suppresses epithelial cell apoptosis and migration. (A) The TUNEL staining in lens sections of AAV-NC and AAV-NR2F1 mice with ASC. Scale bar: 50 μm. (B – D) The protein levels and quantitative charts of BAX and CASP3 in the two groups mentioned above. n = 3 per group; mean ± standard deviation; ∗ p < 0.05, ∗∗ p < 0.01; unpaired student's t -test. (E, F) The TUNEL staining in the TGF-β1-mediated group with Sh-NR2F1 compared with that with Sh-NC. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test; scale bar, 200 μm. (G – I) The protein expression and quantification of BAX and CASP3 in TGF-β1-induced SRA01/04 cells with or without Sh-NR2F1. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test. (J, K) The transwell assay in the two groups mentioned above. n = 4 per group; mean ± standard deviation; ∗∗ p < 0.01; unpaired student's t -test. (I–K) The protein expression and quantification of BAX and CASP3 in TGF-β1-induced SRA01/04 cells with or without Sh-NR2F1. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test. NR2F1, nuclear receptor subfamily 2 group F member 1; AAV, adeno-associated adenovirus; ASC, anterior subcapsular cataract; BAX, Bcl-2-associated X; CASP3, caspase 3; TGF-β1, transforming growth factor-β1.

Journal: Genes & Diseases

Article Title: Autophagy-induced NR2F1 activation promotes the apoptosis of lens epithelial cells and facilitates cataract-associated fibrosis through targeting STAT3

doi: 10.1016/j.gendis.2025.101549

Figure Lengend Snippet: NR2F1 inhibition suppresses epithelial cell apoptosis and migration. (A) The TUNEL staining in lens sections of AAV-NC and AAV-NR2F1 mice with ASC. Scale bar: 50 μm. (B – D) The protein levels and quantitative charts of BAX and CASP3 in the two groups mentioned above. n = 3 per group; mean ± standard deviation; ∗ p < 0.05, ∗∗ p < 0.01; unpaired student's t -test. (E, F) The TUNEL staining in the TGF-β1-mediated group with Sh-NR2F1 compared with that with Sh-NC. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test; scale bar, 200 μm. (G – I) The protein expression and quantification of BAX and CASP3 in TGF-β1-induced SRA01/04 cells with or without Sh-NR2F1. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test. (J, K) The transwell assay in the two groups mentioned above. n = 4 per group; mean ± standard deviation; ∗∗ p < 0.01; unpaired student's t -test. (I–K) The protein expression and quantification of BAX and CASP3 in TGF-β1-induced SRA01/04 cells with or without Sh-NR2F1. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; unpaired student's t -test. NR2F1, nuclear receptor subfamily 2 group F member 1; AAV, adeno-associated adenovirus; ASC, anterior subcapsular cataract; BAX, Bcl-2-associated X; CASP3, caspase 3; TGF-β1, transforming growth factor-β1.

Article Snippet: NR2F1 agonist 1 (HY-149913, MCE) was treated at 0.5 or 1 μM concentration.

Techniques: Inhibition, Migration, TUNEL Assay, Staining, Standard Deviation, Expressing, Transwell Assay

NR2F1 directly binds to STAT3 and regulates the expression of p-STAT3. (A, B) The protein levels and quantification of JAK1, p-STAT3, SMAD2, and MYD88 in TGF-β1-treated SRA01/04 cells with or without Sh-NR2F1. n = 3 per group; mean ± standard deviation; ns, >0.05; ∗∗ p < 0.01; unpaired student's t -test. (C, D) The protein level and quantitative chart of p-STAT3 in AAV-NC or AAV-NR2F1 ASC mice. n = 3 per group; mean ± standard deviation; ∗ p < 0.01; unpaired student's t -test. (E) The motif of NR2F1 predicted by the JASPAR website. (F) A dual-luciferase vector. (G) Mutant and wild-type STAT3 plasmids consequences. (H) The dual-luciferase assay for NR2F1 and STAT3 promoter. n = 3 per group; mean ± standard deviation; ns, >0.05; ∗ p < 0.05; unpaired student's t -test. (I, J) The protein level of p-STAT3 in TGF-β1-induced SRA01/04 cells following NR2F1 agonist treatment at 0.5 or 1 μM. n = 3 per group; mean ± standard deviation; ns > 0.05; ∗ p < 0.05; one-way ANOVA. (K) Structure of p-STAT3 specific inhibitor NSC 74859. (L, M) The protein expression and quantification of p-STAT3, STAT3, JAK1, FN1, VIM, and α-SMA in TGF-β1-induced SRA01/04 cells treated with the specific P-STAT3 inhibitor. n = 3 per group; mean ± standard deviation; ns, >0.05, ∗ p < 0.05, ∗∗ p < 0.01; one-way ANOVA. (N, O) The protein expression of the apoptosis-related markers BAX and CASP3 in TGF-β1-induced SRA01/04 cells treated with NSC 74859. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; one-way ANOVA. NR2F1, nuclear receptor subfamily 2 group F member 1; STAT3, signal transducer and activator of transcription 3; p-STAT3, phosphorylated STAT3; ASC, anterior subcapsular cataract; FN1, fibronectin 1; α-SMA, α-smooth muscle actin; VIM, vimentin; BAX, Bcl-2-associated X; CASP3, caspase 3; TGF-β1, transforming growth factor-β1; JAK1, Janus kinase 1; SMAD2, SMAD family member 2; AAV, adeno-associated adenovirus.

Journal: Genes & Diseases

Article Title: Autophagy-induced NR2F1 activation promotes the apoptosis of lens epithelial cells and facilitates cataract-associated fibrosis through targeting STAT3

doi: 10.1016/j.gendis.2025.101549

Figure Lengend Snippet: NR2F1 directly binds to STAT3 and regulates the expression of p-STAT3. (A, B) The protein levels and quantification of JAK1, p-STAT3, SMAD2, and MYD88 in TGF-β1-treated SRA01/04 cells with or without Sh-NR2F1. n = 3 per group; mean ± standard deviation; ns, >0.05; ∗∗ p < 0.01; unpaired student's t -test. (C, D) The protein level and quantitative chart of p-STAT3 in AAV-NC or AAV-NR2F1 ASC mice. n = 3 per group; mean ± standard deviation; ∗ p < 0.01; unpaired student's t -test. (E) The motif of NR2F1 predicted by the JASPAR website. (F) A dual-luciferase vector. (G) Mutant and wild-type STAT3 plasmids consequences. (H) The dual-luciferase assay for NR2F1 and STAT3 promoter. n = 3 per group; mean ± standard deviation; ns, >0.05; ∗ p < 0.05; unpaired student's t -test. (I, J) The protein level of p-STAT3 in TGF-β1-induced SRA01/04 cells following NR2F1 agonist treatment at 0.5 or 1 μM. n = 3 per group; mean ± standard deviation; ns > 0.05; ∗ p < 0.05; one-way ANOVA. (K) Structure of p-STAT3 specific inhibitor NSC 74859. (L, M) The protein expression and quantification of p-STAT3, STAT3, JAK1, FN1, VIM, and α-SMA in TGF-β1-induced SRA01/04 cells treated with the specific P-STAT3 inhibitor. n = 3 per group; mean ± standard deviation; ns, >0.05, ∗ p < 0.05, ∗∗ p < 0.01; one-way ANOVA. (N, O) The protein expression of the apoptosis-related markers BAX and CASP3 in TGF-β1-induced SRA01/04 cells treated with NSC 74859. n = 3 per group; mean ± standard deviation; ∗ p < 0.05; one-way ANOVA. NR2F1, nuclear receptor subfamily 2 group F member 1; STAT3, signal transducer and activator of transcription 3; p-STAT3, phosphorylated STAT3; ASC, anterior subcapsular cataract; FN1, fibronectin 1; α-SMA, α-smooth muscle actin; VIM, vimentin; BAX, Bcl-2-associated X; CASP3, caspase 3; TGF-β1, transforming growth factor-β1; JAK1, Janus kinase 1; SMAD2, SMAD family member 2; AAV, adeno-associated adenovirus.

Article Snippet: NR2F1 agonist 1 (HY-149913, MCE) was treated at 0.5 or 1 μM concentration.

Techniques: Expressing, Standard Deviation, Luciferase, Plasmid Preparation, Mutagenesis

The regulatory mechanism of NR2F1 in TGF-β1-induced SRA01/04 cells. NR2F1, nuclear receptor subfamily 2 group F member 1; TGF-β1, transforming growth factor-β1.

Journal: Genes & Diseases

Article Title: Autophagy-induced NR2F1 activation promotes the apoptosis of lens epithelial cells and facilitates cataract-associated fibrosis through targeting STAT3

doi: 10.1016/j.gendis.2025.101549

Figure Lengend Snippet: The regulatory mechanism of NR2F1 in TGF-β1-induced SRA01/04 cells. NR2F1, nuclear receptor subfamily 2 group F member 1; TGF-β1, transforming growth factor-β1.

Article Snippet: NR2F1 agonist 1 (HY-149913, MCE) was treated at 0.5 or 1 μM concentration.

Techniques:

(A) Schematics demarcating the locations of the cranial neural crest-producing neural plate border (green in 1–2 somite stage (ss) embryo), specified cranial neural crest (cNC) (green in ~3, 4–5, and 8–12ss embryos), cranial mesoderm (pink), and lateral plate mesoderm (plum) during early cNC development. (B) Dorsal and lateral views of in situ hybridizations for Nr2f1 (Ba-c′,j-l) and Nr2f2 (Bd-f’,m-o) compared with Tfap2a (marking cNC and non-neural ectoderm and anterior preplacodal ectoderm, Bg-i’,p-r). Black arrowheads in Ba and double arrowhead in Bj mark Nr2f1 expression at 1–2ss and in nascent PA1 at 6ss, respectively. Black arrows in Bj′, Bm′ indicate Nr2f1 and Nr2f2 expression domains in the neural plate at 6ss. (C) The Nr2f2 flox allele contains a lacZ cassette activated upon Cre-mediated recombination, which was used to exclude obfuscating expression of Nr2f2 in the facial ectoderm and cranial mesoderm. X-gal treatment of Wnt1-Cre;Nr2f2-lacZ embryos revealed no cNC-specific activity at 6–7ss (Ca), patchy staining at 8–9ss (Cb), and robust staining at 9–12ss (Cc-d). (D) Post-migratory expression of Nr2f1/2 and Tfap2a at E9.5–10.5. (Da-b, Dd-e) Nr2f1 and Nr2f2 are expressed in the mandibular prominence and the posterior portion of the maxillary prominence at E9.5 and E10.5. White arrowheads mark the maxillary domain; white arrow in Db marks Nr2f2 expression in arch ectoderm. (Dc,f) At these stages, Tfap2a expression persists only in the frontonasal prominence, arch ectoderm, and the forming trigeminal ganglion (double arrowheads). (E) Immunofluorescence showing serial sections stained for NR2F1 (Ea-d), NR2F2 (Ee-h), and SOX9 (marking premigratory and migratory crest) (Ei-l). White arrowheads (Ea,i) mark NR2F1- and SOX9-expressing neural plate border. Scale bars = 1 mm except in E where scale bars = 100 mm. n≥3 for all panels, except Bd where n=2.

Journal: Developmental biology

Article Title: Cranial neural crest shortage leads to extensive craniofacial anomalies in mice mutant for the NR2F1/2 nuclear receptors

doi: 10.1016/j.ydbio.2025.11.011

Figure Lengend Snippet: (A) Schematics demarcating the locations of the cranial neural crest-producing neural plate border (green in 1–2 somite stage (ss) embryo), specified cranial neural crest (cNC) (green in ~3, 4–5, and 8–12ss embryos), cranial mesoderm (pink), and lateral plate mesoderm (plum) during early cNC development. (B) Dorsal and lateral views of in situ hybridizations for Nr2f1 (Ba-c′,j-l) and Nr2f2 (Bd-f’,m-o) compared with Tfap2a (marking cNC and non-neural ectoderm and anterior preplacodal ectoderm, Bg-i’,p-r). Black arrowheads in Ba and double arrowhead in Bj mark Nr2f1 expression at 1–2ss and in nascent PA1 at 6ss, respectively. Black arrows in Bj′, Bm′ indicate Nr2f1 and Nr2f2 expression domains in the neural plate at 6ss. (C) The Nr2f2 flox allele contains a lacZ cassette activated upon Cre-mediated recombination, which was used to exclude obfuscating expression of Nr2f2 in the facial ectoderm and cranial mesoderm. X-gal treatment of Wnt1-Cre;Nr2f2-lacZ embryos revealed no cNC-specific activity at 6–7ss (Ca), patchy staining at 8–9ss (Cb), and robust staining at 9–12ss (Cc-d). (D) Post-migratory expression of Nr2f1/2 and Tfap2a at E9.5–10.5. (Da-b, Dd-e) Nr2f1 and Nr2f2 are expressed in the mandibular prominence and the posterior portion of the maxillary prominence at E9.5 and E10.5. White arrowheads mark the maxillary domain; white arrow in Db marks Nr2f2 expression in arch ectoderm. (Dc,f) At these stages, Tfap2a expression persists only in the frontonasal prominence, arch ectoderm, and the forming trigeminal ganglion (double arrowheads). (E) Immunofluorescence showing serial sections stained for NR2F1 (Ea-d), NR2F2 (Ee-h), and SOX9 (marking premigratory and migratory crest) (Ei-l). White arrowheads (Ea,i) mark NR2F1- and SOX9-expressing neural plate border. Scale bars = 1 mm except in E where scale bars = 100 mm. n≥3 for all panels, except Bd where n=2.

Article Snippet: The Nr2f1 tm2.1Mjts/Mmmh ( Nr2f1 flox ; RRID:MMRRC_032804-MU; Tang et al., 2010 ) and Nr2f2 tm2.1Tsa/Mmmh ( Nr2f2 flox ; RRID:MMRRC_032805-MU; Takamoto et al., 2005 ) lines were obtained from the Mutant Mouse Resource and Research Center (MMRRC) in 2016.

Techniques: In Situ, Expressing, Activity Assay, Staining, Immunofluorescence

(A) Schematic summarizing ordered allelic series of Nr2f1/2 cKO jaw phenotypes, excluding double mutants. Lost/reduced jaw/middle ear structures in purple. (B, C, E) Alcian blue and Alizarin red staining of pre- and perinatal skulls shows dose-dependent effects of Nr2f1/2 loss by Wnt1 -Cre. (B) No phenotypes are apparent in P0 Wnt1-Cre;Nr2f1 flox/flox conditional mutants (Bb) relative to controls (Ba), and only mild phenotypes in Wnt1-Cre;Nr2f2 flox/flox conditional mutants (Bc), most notably the previously reported branched tympanic ring (bordered arrowhead)( Hsu et al. 2017 ). (C) Lateral, dorsal, and ventral views of skulls of the indicated genotypes are shown in the top three rows of C; the fourth row shows dissected upper and lower jaws. Dissected middle ear complexes are shown in E. Asterisks in C indicate reduction of the alisphenoid (al) in the third row and reduction of the zygomatic process of the maxilla (mx), jugal (j), and squamosal (sq) bones in the fourth row. Black arrowheads indicate progressive reduction of the coronal and angular processes of the mandible. Black arrow in Cp indicates the remnant palatal process of the premaxilla (pmx) in the Wnt1-Cre;Nr2f1 flox/flox ; Nr2f2 flox/flox specimen. White arrowheads in E indicate branched and/or truncated tympanic rings. Black stars in Ck-o mark subtle cleft palate in Wnt1-Cre;Nr2f1 flox /+ ; Nr2f2 flox/flox mutants involving disunion of the palatine bones, and total absence of palatal tissue and splitting of the vomer in Wnt1-Cre;Nr2f1 flox/flox ; Nr2f2 flox/flox double mutants. (D) Appearance of Wnt1-Cre;Nr2f1 flox/flox ; Nr2f2 flox/flox mutant and control heads at E18.5. Note the brain appearing to protrude beyond the severely cleft midface (Dd-e), the minimal tissue between the brain and tongue (white asterisk in Df), and the anteriorly displaced pinna (white arrow in Dd). Scale bars = 1 mm in all panels. n values are indicated in each panel showing lateral images.

Journal: Developmental biology

Article Title: Cranial neural crest shortage leads to extensive craniofacial anomalies in mice mutant for the NR2F1/2 nuclear receptors

doi: 10.1016/j.ydbio.2025.11.011

Figure Lengend Snippet: (A) Schematic summarizing ordered allelic series of Nr2f1/2 cKO jaw phenotypes, excluding double mutants. Lost/reduced jaw/middle ear structures in purple. (B, C, E) Alcian blue and Alizarin red staining of pre- and perinatal skulls shows dose-dependent effects of Nr2f1/2 loss by Wnt1 -Cre. (B) No phenotypes are apparent in P0 Wnt1-Cre;Nr2f1 flox/flox conditional mutants (Bb) relative to controls (Ba), and only mild phenotypes in Wnt1-Cre;Nr2f2 flox/flox conditional mutants (Bc), most notably the previously reported branched tympanic ring (bordered arrowhead)( Hsu et al. 2017 ). (C) Lateral, dorsal, and ventral views of skulls of the indicated genotypes are shown in the top three rows of C; the fourth row shows dissected upper and lower jaws. Dissected middle ear complexes are shown in E. Asterisks in C indicate reduction of the alisphenoid (al) in the third row and reduction of the zygomatic process of the maxilla (mx), jugal (j), and squamosal (sq) bones in the fourth row. Black arrowheads indicate progressive reduction of the coronal and angular processes of the mandible. Black arrow in Cp indicates the remnant palatal process of the premaxilla (pmx) in the Wnt1-Cre;Nr2f1 flox/flox ; Nr2f2 flox/flox specimen. White arrowheads in E indicate branched and/or truncated tympanic rings. Black stars in Ck-o mark subtle cleft palate in Wnt1-Cre;Nr2f1 flox /+ ; Nr2f2 flox/flox mutants involving disunion of the palatine bones, and total absence of palatal tissue and splitting of the vomer in Wnt1-Cre;Nr2f1 flox/flox ; Nr2f2 flox/flox double mutants. (D) Appearance of Wnt1-Cre;Nr2f1 flox/flox ; Nr2f2 flox/flox mutant and control heads at E18.5. Note the brain appearing to protrude beyond the severely cleft midface (Dd-e), the minimal tissue between the brain and tongue (white asterisk in Df), and the anteriorly displaced pinna (white arrow in Dd). Scale bars = 1 mm in all panels. n values are indicated in each panel showing lateral images.

Techniques: Staining, Mutagenesis, Control

(A-C) PAX3 (A) is expressed in the neural plate border more broadly than premigratory neural crest marker SOX9 (B); merged images shown in C. Compared with sibling controls (D-F), 3/3 Pax3 Cre dcKOs (G-I) present with craniofacial phenotypes similar to those of the Wnt1- Cre dcKOs, including preservation of the distal mandible (compare asterisks, arrowheads, arrow in Figs. 2Cp and 3I ). Scale bars = 100 μm in A-C and 1 mm in D-I.

Journal: Developmental biology

Article Title: Cranial neural crest shortage leads to extensive craniofacial anomalies in mice mutant for the NR2F1/2 nuclear receptors

doi: 10.1016/j.ydbio.2025.11.011

Figure Lengend Snippet: (A-C) PAX3 (A) is expressed in the neural plate border more broadly than premigratory neural crest marker SOX9 (B); merged images shown in C. Compared with sibling controls (D-F), 3/3 Pax3 Cre dcKOs (G-I) present with craniofacial phenotypes similar to those of the Wnt1- Cre dcKOs, including preservation of the distal mandible (compare asterisks, arrowheads, arrow in Figs. 2Cp and 3I ). Scale bars = 100 μm in A-C and 1 mm in D-I.

Techniques: Generated, Marker, Preserving

(A-C) Immunofluorescence for Cre (a-c panels; magenta) compared with SOX9 (d-f panels; green); merged images shown in g-i panels. At 1–2ss, when SOX9 protein begins to be enriched at the neural plate border, nuclear-localized Cre protein is already detectable in 2/7 Wnt1-Cre + but 0/3 Pax3 Cre + embryos (Ab-c). In 3–4ss and 4–5ss embryos (B-C), robust nuclear Cre expression is evident in 5/5 and 2/3 Wnt1-Cre + embryos, respectively (Bb,Cb), and in 4/5 and 4/4 Pax3 Cre + embryos, respectively (Bc,Cc). (D) When recombined with Wnt1 -Cre, the R26R-EYFP reporter is absent at 0–1ss (Da) but detectable by 1–2ss (Db) and more strongly thereafter (Dc-f). Nuclei stained with DAPI. (E-G) Immunofluorescence for Cre (magenta) and NR2F1 (green). (E) At 1–2ss, 5/6 Wnt1-Cre+ Nr2f1 cKO embryos assessed for NR2F1 were positive (Eb), and no reduction in protein was visible. (F) At ~3ss, compared with the control (Fd, arrowhead), 3/4 Nr2f1 cKOs (Fe, arrowhead) have already lost most NR2F1 protein in Cre+ cells (compare to arrow-marked NR2F1+ ectoderm); 1/4 (Ff, arrowhead) retained a normal level. (G) By 4–5ss, no NR2F1 is visible in Cre+ cells in Nr2f1 cKOs (3/3; compare Ge to Gd). (H) Schematic showing proposed onset of Wnt1-Cre and Pax3 Cre Cre protein expression (blue and purple, respectively) with proposed timing of NR2F1 loss after Wnt1-Cre ablation compared to persistent expression in control (green). Scale bars = 100 mm. n≥3 for all controls. Note that the control embryo displayed in Ca,d,g is the same as Ga,d,g, and the Wnt1-Cre + embryo in Ab,e,h is the same as the one displayed in Ea-c.

Journal: Developmental biology

Article Title: Cranial neural crest shortage leads to extensive craniofacial anomalies in mice mutant for the NR2F1/2 nuclear receptors

doi: 10.1016/j.ydbio.2025.11.011

Figure Lengend Snippet: (A-C) Immunofluorescence for Cre (a-c panels; magenta) compared with SOX9 (d-f panels; green); merged images shown in g-i panels. At 1–2ss, when SOX9 protein begins to be enriched at the neural plate border, nuclear-localized Cre protein is already detectable in 2/7 Wnt1-Cre + but 0/3 Pax3 Cre + embryos (Ab-c). In 3–4ss and 4–5ss embryos (B-C), robust nuclear Cre expression is evident in 5/5 and 2/3 Wnt1-Cre + embryos, respectively (Bb,Cb), and in 4/5 and 4/4 Pax3 Cre + embryos, respectively (Bc,Cc). (D) When recombined with Wnt1 -Cre, the R26R-EYFP reporter is absent at 0–1ss (Da) but detectable by 1–2ss (Db) and more strongly thereafter (Dc-f). Nuclei stained with DAPI. (E-G) Immunofluorescence for Cre (magenta) and NR2F1 (green). (E) At 1–2ss, 5/6 Wnt1-Cre+ Nr2f1 cKO embryos assessed for NR2F1 were positive (Eb), and no reduction in protein was visible. (F) At ~3ss, compared with the control (Fd, arrowhead), 3/4 Nr2f1 cKOs (Fe, arrowhead) have already lost most NR2F1 protein in Cre+ cells (compare to arrow-marked NR2F1+ ectoderm); 1/4 (Ff, arrowhead) retained a normal level. (G) By 4–5ss, no NR2F1 is visible in Cre+ cells in Nr2f1 cKOs (3/3; compare Ge to Gd). (H) Schematic showing proposed onset of Wnt1-Cre and Pax3 Cre Cre protein expression (blue and purple, respectively) with proposed timing of NR2F1 loss after Wnt1-Cre ablation compared to persistent expression in control (green). Scale bars = 100 mm. n≥3 for all controls. Note that the control embryo displayed in Ca,d,g is the same as Ga,d,g, and the Wnt1-Cre + embryo in Ab,e,h is the same as the one displayed in Ea-c.

Techniques: Immunofluorescence, Expressing, Staining, Control

(A-B) Colorimetric in situs for Dlx5 at E10.5 reveal hypoplasia of PA1 and PA2 in Wnt1-Cre dcKOs, with the core of Dlx5 -negative mesoderm exposed. (C-F) Dlx2 expression at E10.5 (C-D) and E9.5 (E-F) supports disproportionate reduction of the MxP. (G) Schematic highlighting difference in PA1 size, color coded with an interpretation of maxillary (green) and mandibular (pink) domains in dcKOs and controls derived from A-D. (H-O) Wnt1- Cre-converted cNC (white) were traced with the ccEGFP Cre reporter. (H-K) At E10.5 and E9.5, the MdP is hypoplastic, and almost no EGFP+ cells are visible in the MxP. Brackets outlining the control FNP in (H) and replicated in the dcKO (I) reveal the reduced size of the latter at E10.5. Asterisks (H-K) mark likely trigeminal ganglia precursors. Note the split precursor populations and massive depletion in dcKOs. Arrows (H-K) point to the boundary between PA1 and PA2, which loses definition in dcKOs. (L-M) At 16ss (~E8.75), brackets and arrows show underdevelopment of the MdP and few cells in the MxP, respectively. (N-O) At 14ss, 2/3 dcKOs present with a mildly reduced migrating stream (double arrows). Scale bars = 1 mm.

Journal: Developmental biology

Article Title: Cranial neural crest shortage leads to extensive craniofacial anomalies in mice mutant for the NR2F1/2 nuclear receptors

doi: 10.1016/j.ydbio.2025.11.011

Figure Lengend Snippet: (A-B) Colorimetric in situs for Dlx5 at E10.5 reveal hypoplasia of PA1 and PA2 in Wnt1-Cre dcKOs, with the core of Dlx5 -negative mesoderm exposed. (C-F) Dlx2 expression at E10.5 (C-D) and E9.5 (E-F) supports disproportionate reduction of the MxP. (G) Schematic highlighting difference in PA1 size, color coded with an interpretation of maxillary (green) and mandibular (pink) domains in dcKOs and controls derived from A-D. (H-O) Wnt1- Cre-converted cNC (white) were traced with the ccEGFP Cre reporter. (H-K) At E10.5 and E9.5, the MdP is hypoplastic, and almost no EGFP+ cells are visible in the MxP. Brackets outlining the control FNP in (H) and replicated in the dcKO (I) reveal the reduced size of the latter at E10.5. Asterisks (H-K) mark likely trigeminal ganglia precursors. Note the split precursor populations and massive depletion in dcKOs. Arrows (H-K) point to the boundary between PA1 and PA2, which loses definition in dcKOs. (L-M) At 16ss (~E8.75), brackets and arrows show underdevelopment of the MdP and few cells in the MxP, respectively. (N-O) At 14ss, 2/3 dcKOs present with a mildly reduced migrating stream (double arrows). Scale bars = 1 mm.

Techniques: Migration, Expressing, Derivative Assay, Control

(A) Schematic showing head tissue collection strategy for RNAseq and summarized results. More differentially expressed genes (DEGs) were identified at 12ss vs. 8ss. (B-C) Volcano plots showing DEGs (pink) from 8 and 12ss samples. Dashed lines demarcate p adj <0.05 and log2 fold change>0.585 (i.e. 1.5 fold change). (D) cNC-associated DEGs at 12ss. FC was derived from absolute values of log2 fold change output from DESeq2. (E-F) WMISH showing reduced expression of Twist1 in the Wnt1-Cre dcKO at 14ss (n=1; * similar findings at 10ss; n=1, and 20ss; n=3 for both dcKOs and controls). (G-H) Sox10 expression is reduced in dcKO migrating crest at 16ss (n=3; similar findings at 10ss and ~20ss; n=1 ea. for both dcKOs and controls). Note similar levels of expression in the otic vesicle (arrowheads). (I-J) Expression of Plcg2 is completely lost in the 16ss dcKO (n=2). Note Plcg2 is one of the most strongly downregulated genes. (K-N) Expression of Plcg2 in wild-type embryos via WMISH. (O) scRNAseq data (published in Soldatov et al. (2019) and publicly available at http://pklab.med.harvard.edu/cgi-bin/R/rook/nc.cranial_E85/index.html ) comparing expression of Plcg2, Nr2f2, Twist1 , and Sox10 in E8.5 cNC. Note the more gradual onset of expression of Plcg2 , Nr2f2 , and Twist1 compared to Sox10 . (P) Schematic depicting NR2F1/2 ChIP peak from Rada-Iglesias et al. (2012) overlapping with an ENCODE candidate cis-regulatory element and a candidate neural crest-specific enhancer ~48kb upstream of human PLCG2. This element is conserved in mice ~28kb upstream of Plcg2 . Scale bars = 1 mm.

Journal: Developmental biology

Article Title: Cranial neural crest shortage leads to extensive craniofacial anomalies in mice mutant for the NR2F1/2 nuclear receptors

doi: 10.1016/j.ydbio.2025.11.011

Figure Lengend Snippet: (A) Schematic showing head tissue collection strategy for RNAseq and summarized results. More differentially expressed genes (DEGs) were identified at 12ss vs. 8ss. (B-C) Volcano plots showing DEGs (pink) from 8 and 12ss samples. Dashed lines demarcate p adj <0.05 and log2 fold change>0.585 (i.e. 1.5 fold change). (D) cNC-associated DEGs at 12ss. FC was derived from absolute values of log2 fold change output from DESeq2. (E-F) WMISH showing reduced expression of Twist1 in the Wnt1-Cre dcKO at 14ss (n=1; * similar findings at 10ss; n=1, and 20ss; n=3 for both dcKOs and controls). (G-H) Sox10 expression is reduced in dcKO migrating crest at 16ss (n=3; similar findings at 10ss and ~20ss; n=1 ea. for both dcKOs and controls). Note similar levels of expression in the otic vesicle (arrowheads). (I-J) Expression of Plcg2 is completely lost in the 16ss dcKO (n=2). Note Plcg2 is one of the most strongly downregulated genes. (K-N) Expression of Plcg2 in wild-type embryos via WMISH. (O) scRNAseq data (published in Soldatov et al. (2019) and publicly available at http://pklab.med.harvard.edu/cgi-bin/R/rook/nc.cranial_E85/index.html ) comparing expression of Plcg2, Nr2f2, Twist1 , and Sox10 in E8.5 cNC. Note the more gradual onset of expression of Plcg2 , Nr2f2 , and Twist1 compared to Sox10 . (P) Schematic depicting NR2F1/2 ChIP peak from Rada-Iglesias et al. (2012) overlapping with an ENCODE candidate cis-regulatory element and a candidate neural crest-specific enhancer ~48kb upstream of human PLCG2. This element is conserved in mice ~28kb upstream of Plcg2 . Scale bars = 1 mm.

Techniques: Derivative Assay, Expressing

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