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anti snail2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti snail2
    Anti Snail2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1309 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+slug+snail2/bio_rxiv__2025__09__06__674616-99-50-52?v=Cell+Signaling+Technology+Inc
    Average 96 stars, based on 1309 article reviews
    anti snail2 - by Bioz Stars, 2026-07
    96/100 stars

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    Figure 3. Differential neural crest behavior underlies the acquisition of a thinned-out and expanded dorsal hindbrain roof (A) Confocal images of actin and phosphorylated myosin light chain kinase II in the hindbrain and spinal cord of HH12 stage embryos. (B and C) Quantification of apical actin signal intensity along the lumen circumference in the hindbrain and spinal cord of HH11-HH12 stage embryos (n = 3) (p = 0.012 and 0.53, paired t tests). (D) Confocal images showing <t>Snail2+</t> cell migration in the hindbrain and spinal cord cross sections of embryos progressing toward brain-expansion stages (HH9 to HH12). (E) Confocal images showing laminin and actin organization in cross-section views of the hindbrain and spinal cord of HH12 stage embryos. (F) Confocal images showing laminin organization at the dorsal surface in a 3D rendering of the hindbrain and spinal cord of HH11 stage embryos. (G) Bright-field images of embryos treated with dimethyl sulfoxide (DMSO) or MMP inhibitor at HH11 and incubated for 20 h. Arrows indicate hindbrain at level of otic vesicle. (H) Dorsal views of DMSO- and MMP inhibitor-treated embryos. Yellow highlight fills the brain dorsal surface. (I) Confocal images showing the dorsal hindbrain of control and MMP inhibitor-treated embryos, ∼20 h post treatment. Bottom panels show laminin surface with arrows indicating breaks in laminin continuity. (J) Hindbrain roof length in control (n = 6) and inhibitor-treated (n = 8) embryos (p = 0.0000048, t test). White scale bars are 50 μm unless otherwise stated. See also Figure S3.
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    Figure 3. Differential neural crest behavior underlies the acquisition of a thinned-out and expanded dorsal hindbrain roof (A) Confocal images of actin and phosphorylated myosin light chain kinase II in the hindbrain and spinal cord of HH12 stage embryos. (B and C) Quantification of apical actin signal intensity along the lumen circumference in the hindbrain and spinal cord of HH11-HH12 stage embryos (n = 3) (p = 0.012 and 0.53, paired t tests). (D) Confocal images showing <t>Snail2+</t> cell migration in the hindbrain and spinal cord cross sections of embryos progressing toward brain-expansion stages (HH9 to HH12). (E) Confocal images showing laminin and actin organization in cross-section views of the hindbrain and spinal cord of HH12 stage embryos. (F) Confocal images showing laminin organization at the dorsal surface in a 3D rendering of the hindbrain and spinal cord of HH11 stage embryos. (G) Bright-field images of embryos treated with dimethyl sulfoxide (DMSO) or MMP inhibitor at HH11 and incubated for 20 h. Arrows indicate hindbrain at level of otic vesicle. (H) Dorsal views of DMSO- and MMP inhibitor-treated embryos. Yellow highlight fills the brain dorsal surface. (I) Confocal images showing the dorsal hindbrain of control and MMP inhibitor-treated embryos, ∼20 h post treatment. Bottom panels show laminin surface with arrows indicating breaks in laminin continuity. (J) Hindbrain roof length in control (n = 6) and inhibitor-treated (n = 8) embryos (p = 0.0000048, t test). White scale bars are 50 μm unless otherwise stated. See also Figure S3.
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    Figure 3. Differential neural crest behavior underlies the acquisition of a thinned-out and expanded dorsal hindbrain roof (A) Confocal images of actin and phosphorylated myosin light chain kinase II in the hindbrain and spinal cord of HH12 stage embryos. (B and C) Quantification of apical actin signal intensity along the lumen circumference in the hindbrain and spinal cord of HH11-HH12 stage embryos (n = 3) (p = 0.012 and 0.53, paired t tests). (D) Confocal images showing <t>Snail2+</t> cell migration in the hindbrain and spinal cord cross sections of embryos progressing toward brain-expansion stages (HH9 to HH12). (E) Confocal images showing laminin and actin organization in cross-section views of the hindbrain and spinal cord of HH12 stage embryos. (F) Confocal images showing laminin organization at the dorsal surface in a 3D rendering of the hindbrain and spinal cord of HH11 stage embryos. (G) Bright-field images of embryos treated with dimethyl sulfoxide (DMSO) or MMP inhibitor at HH11 and incubated for 20 h. Arrows indicate hindbrain at level of otic vesicle. (H) Dorsal views of DMSO- and MMP inhibitor-treated embryos. Yellow highlight fills the brain dorsal surface. (I) Confocal images showing the dorsal hindbrain of control and MMP inhibitor-treated embryos, ∼20 h post treatment. Bottom panels show laminin surface with arrows indicating breaks in laminin continuity. (J) Hindbrain roof length in control (n = 6) and inhibitor-treated (n = 8) embryos (p = 0.0000048, t test). White scale bars are 50 μm unless otherwise stated. See also Figure S3.
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    Figure 3. Differential neural crest behavior underlies the acquisition of a thinned-out and expanded dorsal hindbrain roof (A) Confocal images of actin and phosphorylated myosin light chain kinase II in the hindbrain and spinal cord of HH12 stage embryos. (B and C) Quantification of apical actin signal intensity along the lumen circumference in the hindbrain and spinal cord of HH11-HH12 stage embryos (n = 3) (p = 0.012 and 0.53, paired t tests). (D) Confocal images showing <t>Snail2+</t> cell migration in the hindbrain and spinal cord cross sections of embryos progressing toward brain-expansion stages (HH9 to HH12). (E) Confocal images showing laminin and actin organization in cross-section views of the hindbrain and spinal cord of HH12 stage embryos. (F) Confocal images showing laminin organization at the dorsal surface in a 3D rendering of the hindbrain and spinal cord of HH11 stage embryos. (G) Bright-field images of embryos treated with dimethyl sulfoxide (DMSO) or MMP inhibitor at HH11 and incubated for 20 h. Arrows indicate hindbrain at level of otic vesicle. (H) Dorsal views of DMSO- and MMP inhibitor-treated embryos. Yellow highlight fills the brain dorsal surface. (I) Confocal images showing the dorsal hindbrain of control and MMP inhibitor-treated embryos, ∼20 h post treatment. Bottom panels show laminin surface with arrows indicating breaks in laminin continuity. (J) Hindbrain roof length in control (n = 6) and inhibitor-treated (n = 8) embryos (p = 0.0000048, t test). White scale bars are 50 μm unless otherwise stated. See also Figure S3.
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    Image Search Results


    Figure 3. Differential neural crest behavior underlies the acquisition of a thinned-out and expanded dorsal hindbrain roof (A) Confocal images of actin and phosphorylated myosin light chain kinase II in the hindbrain and spinal cord of HH12 stage embryos. (B and C) Quantification of apical actin signal intensity along the lumen circumference in the hindbrain and spinal cord of HH11-HH12 stage embryos (n = 3) (p = 0.012 and 0.53, paired t tests). (D) Confocal images showing Snail2+ cell migration in the hindbrain and spinal cord cross sections of embryos progressing toward brain-expansion stages (HH9 to HH12). (E) Confocal images showing laminin and actin organization in cross-section views of the hindbrain and spinal cord of HH12 stage embryos. (F) Confocal images showing laminin organization at the dorsal surface in a 3D rendering of the hindbrain and spinal cord of HH11 stage embryos. (G) Bright-field images of embryos treated with dimethyl sulfoxide (DMSO) or MMP inhibitor at HH11 and incubated for 20 h. Arrows indicate hindbrain at level of otic vesicle. (H) Dorsal views of DMSO- and MMP inhibitor-treated embryos. Yellow highlight fills the brain dorsal surface. (I) Confocal images showing the dorsal hindbrain of control and MMP inhibitor-treated embryos, ∼20 h post treatment. Bottom panels show laminin surface with arrows indicating breaks in laminin continuity. (J) Hindbrain roof length in control (n = 6) and inhibitor-treated (n = 8) embryos (p = 0.0000048, t test). White scale bars are 50 μm unless otherwise stated. See also Figure S3.

    Journal: Developmental cell

    Article Title: Differential tissue deformability underlies fluid pressure-driven shape divergence of the avian embryonic brain and spinal cord.

    doi: 10.1016/j.devcel.2025.04.010

    Figure Lengend Snippet: Figure 3. Differential neural crest behavior underlies the acquisition of a thinned-out and expanded dorsal hindbrain roof (A) Confocal images of actin and phosphorylated myosin light chain kinase II in the hindbrain and spinal cord of HH12 stage embryos. (B and C) Quantification of apical actin signal intensity along the lumen circumference in the hindbrain and spinal cord of HH11-HH12 stage embryos (n = 3) (p = 0.012 and 0.53, paired t tests). (D) Confocal images showing Snail2+ cell migration in the hindbrain and spinal cord cross sections of embryos progressing toward brain-expansion stages (HH9 to HH12). (E) Confocal images showing laminin and actin organization in cross-section views of the hindbrain and spinal cord of HH12 stage embryos. (F) Confocal images showing laminin organization at the dorsal surface in a 3D rendering of the hindbrain and spinal cord of HH11 stage embryos. (G) Bright-field images of embryos treated with dimethyl sulfoxide (DMSO) or MMP inhibitor at HH11 and incubated for 20 h. Arrows indicate hindbrain at level of otic vesicle. (H) Dorsal views of DMSO- and MMP inhibitor-treated embryos. Yellow highlight fills the brain dorsal surface. (I) Confocal images showing the dorsal hindbrain of control and MMP inhibitor-treated embryos, ∼20 h post treatment. Bottom panels show laminin surface with arrows indicating breaks in laminin continuity. (J) Hindbrain roof length in control (n = 6) and inhibitor-treated (n = 8) embryos (p = 0.0000048, t test). White scale bars are 50 μm unless otherwise stated. See also Figure S3.

    Article Snippet: The following antibodies and dyes where used: Laminin (DSHB, 3H11) 1:100, Snail2 (Cell Signaling Technology, 9585S) 1:200, pMLC2 (Cell Signaling Technology, 3671S) 1:100, Hoechst 1:1000, Phalloidin 647 (Thermo Scientific, A22287) 1:500, Donkey Anti-Mouse 488n IgG (Abcam, ab150105), Donkey Anti-Rabbit 594 (Abcam, ab150076).

    Techniques: Migration, Incubation, Control

    Figure 4. Hindbrain premigratory neural crest cells may be sufficient to generate neural tube expansion under lumen pres- sure (A) Bright-field images of pre-brain-expansion stage embryos with spinal cord-to-spinal cord graft and a hindbrain-to-spinal cord graft. (B and C) Confocal images showing dorsal surface of graft integration ∼20 h post-grafting and cross- sectional views at the levels corresponding to dashed lines in (B). White bracket highlights the thinned-out roof in the graft region. (D) Spinal cord tissue thickness in the region with spinal cord (n = 2) or hindbrain (n = 9) grafted cells. (E) Confocal images showing Snail2+ cells in graft regions. Arrows indicate Snail2+ cells within the GFP+ graft. (F) Model of brain expansion relative to the spinal cord. A greater extent of premigratory neural crest cell mesenchymal behavior and corresponding ECM remodeling underlies a more deformable dorsal roof in the early hindbrain compared with the spinal cord. This allows the hindbrain roof to deform more under internal lumen pressure, driving hindbrain expansion relative to the spinal cord during early embryo development. Black scale bars are 500 μm. White scale bars are 25 μm unless otherwise stated. See also Figure S4.

    Journal: Developmental cell

    Article Title: Differential tissue deformability underlies fluid pressure-driven shape divergence of the avian embryonic brain and spinal cord.

    doi: 10.1016/j.devcel.2025.04.010

    Figure Lengend Snippet: Figure 4. Hindbrain premigratory neural crest cells may be sufficient to generate neural tube expansion under lumen pres- sure (A) Bright-field images of pre-brain-expansion stage embryos with spinal cord-to-spinal cord graft and a hindbrain-to-spinal cord graft. (B and C) Confocal images showing dorsal surface of graft integration ∼20 h post-grafting and cross- sectional views at the levels corresponding to dashed lines in (B). White bracket highlights the thinned-out roof in the graft region. (D) Spinal cord tissue thickness in the region with spinal cord (n = 2) or hindbrain (n = 9) grafted cells. (E) Confocal images showing Snail2+ cells in graft regions. Arrows indicate Snail2+ cells within the GFP+ graft. (F) Model of brain expansion relative to the spinal cord. A greater extent of premigratory neural crest cell mesenchymal behavior and corresponding ECM remodeling underlies a more deformable dorsal roof in the early hindbrain compared with the spinal cord. This allows the hindbrain roof to deform more under internal lumen pressure, driving hindbrain expansion relative to the spinal cord during early embryo development. Black scale bars are 500 μm. White scale bars are 25 μm unless otherwise stated. See also Figure S4.

    Article Snippet: The following antibodies and dyes where used: Laminin (DSHB, 3H11) 1:100, Snail2 (Cell Signaling Technology, 9585S) 1:200, pMLC2 (Cell Signaling Technology, 3671S) 1:100, Hoechst 1:1000, Phalloidin 647 (Thermo Scientific, A22287) 1:500, Donkey Anti-Mouse 488n IgG (Abcam, ab150105), Donkey Anti-Rabbit 594 (Abcam, ab150076).

    Techniques:

    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: Breast cancer cell mesenchymal transition and metastasis directed by DAP5/eIF3d-mediated selective mRNA translation

    doi: 10.1016/j.celrep.2023.112646

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Equal amounts of denatured protein lysates were resolved by SDS-PAGE, transferred to polyvinylidene difluoride (PVDF) membrane, blocked with 5% Bovine Serum Albumin (BSA) for 1 h and incubated at 4°C overnight with primary antibodies at 1:1000 dilution against DAP5 (610742; BD Biosciences, Franklin Lakes, NJ, USA), eIF3D (A301–758A; Bethyl Laboratories Inc., Montgomery, TX, USA), E-Cadherin (3195; Cell Signaling Technology), Claudin-1 (ab15098; Abcam, Cambridge, UK), Snail1 (3895; Cell Signaling Technology), Snail2/Slug (9585; Cell Signaling Technology, Danvers, MA, USA), Twist1 (ab50581; Abcam, Cambridge, UK), Zeb1 (A00548–1; BosterBio, Pleasanton, CA, USA), N-Cadherin (610920; BD Biosciences), Vimentin (ab20346; Abcam), eIF4GI (2858, Cell Signaling Technology), MMP1 (ab137332, Abcam), MMP3 (ab52915, Abcam), GAPDH (2118S, Cell Signaling Technology), β-actin (4967; Cell Signaling Technology).

    Techniques: Recombinant, Staining, Protease Inhibitor, Virus, Reverse Transcription, SYBR Green Assay, Bicinchoninic Acid Protein Assay, MTT Assay, Software, Imaging

    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: Breast cancer cell mesenchymal transition and metastasis directed by DAP5/eIF3d-mediated selective mRNA translation

    doi: 10.1016/j.celrep.2023.112646

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Rabbit monoclonal anti-human/mouse Snail2/Slug antibody , Cell Signaling Technology , Cat# 9585/RRID:AB_2239535.

    Techniques: Recombinant, Staining, Protease Inhibitor, Virus, Reverse Transcription, SYBR Green Assay, Bicinchoninic Acid Protein Assay, MTT Assay, Software, Imaging