Journal: Development (Cambridge, England)

Article Title: TIE1 dependent lymphatic vascular remodeling is mediated by its second tyrosine kinase domain.

doi: 10.1242/dev.204469

Figure Lengend Snippet: Fig.10. FOXC2 expression was abolished in Tie1 deficient lymphatics but restored

Article Snippet: Primary antibodies for immunohistochemistry Antibody Supplier Catalogue # Application Goat anti-mouse VEGFR3 R&D Systems AF743 1:50 Goat anti-human TIE1 R&D Systems AF619 1:100 Goat anti-mouse TIE2 R&D Systems AF762 1:200 Goat anti-mouse integrinα9 R&D Systems AF3827 1:50 Goat anti-VE-Cadherin R&D Systems AF1002 1:400 Goat anti-human Prox1 R&D Systems AF2727 1:100 Sheep anti-mouse FOXC2 R&D Systems AF6989 1:200 Rabbit anti-GFP Invitrogen A11122 1:200 Rabbit anti-FOXO1 Cell Signaling 2880 1:200 Rabbit anti-Lyve1 abcam Ab14917 1:800 Rabbit anti-Prox1 abcam Ab37128 1:250 Rat anti-mouse CD31 PD Pharmingen 557355 1:200 Rat anti-endomucin abcam ab106100 1:200 Development: doi:10.1242/dev.204469: Supplementary information D ev el o pm en t • S up pl em en ta ry in fo rm at io n

Techniques: Expressing

Journal: Cell reports

Article Title: VE-Cadherin Is Required for Lymphatic Valve Formation and Maintenance

doi: 10.1016/j.celrep.2019.07.072

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Mouse monoclonal anti-Foxc2 , Santa Cruz , Cat# SC-515234;.

Techniques: Virus, Recombinant, SYBR Green Assay, cDNA Synthesis, Bicinchoninic Acid Protein Assay, Software

Journal: The Journal of Experimental Medicine

Article Title: Human venous valve disease caused by mutations in FOXC2 and GJC2

doi: 10.1084/jem.20160875

Figure Lengend Snippet: Human VV phenotypes. (A) VVs (arrowheads) were visualized in controls and in patients carrying mutations in the indicated genes, without (left) and with (right) power Doppler imaging of blood flow during a calf squeeze. An asterisk (*) marks stagnant/reversed flow in a VV sinus. Blood flow is from left to right. Bars, 1 mm. (B and C) Number (B) and length (C) of VV identified in patients carrying mutations in FOXC2 ( n = 8 patients), GJC2 ( n = 3), GJA1 ( n = 1), and healthy controls ( n = 10). See Tables S1, S2, and S3. ***, P < 0.0005 (ANOVA with Bonferroni correction). Error bars represent means ± SEM. (D) Immunolocalization (arrowheads) of FOXC2 and CX43 in adult human VV leaflets. Bar, 20 µm. Mut, mutation.

Article Snippet: Antibodies were raised in rabbits to Cx43 (3512; Cell Signaling Technology), sheep to FOXC2 (AF5044; R&D Systems), Foxc2 (AF6989; R&D Systems), and goat to Integrinα9 (BAF3827; R&D Systems).

Techniques: Imaging, Mutagenesis

Journal: The Journal of Experimental Medicine

Article Title: Human venous valve disease caused by mutations in FOXC2 and GJC2

doi: 10.1084/jem.20160875

Figure Lengend Snippet: Connexins pattern valve organization at P0. (A–F) Expression in WT mice (A, C, and E) and the KO or conditional deletion loss-of-function phenotypes at P0 for Gja4 , Gja1 , and Gjc2 (B, D, and F). (A) Immunolocalization of Cx37 (arrowheads), and (B) of Prox1 hi VFCs (arrowheads) in Gja4 −/− mice. Immunolocalization of Cx43 (arrowheads; C), and of Prox1 hi VFCs (arrowhead; D) in Prox1CreER T2 ;Gja1 lx/lx mice after induction of deletion at E15. (E and F) Immunolocalization of GFP (green, arrowheads in E) in Gjc2 GFP/+ reporter mice (E), and of Prox1 hi VFCs (arrowheads in F) in Gjc2 GFP/GFP KO mice (F). n ≥ 6 for all images. Bars, 20 µm. Blood flow is from left to right throughout. Graphs in B, D, and F show the proportion of VVs identified at stage 0 (white) and stage 1 (gray) at P0 for the indicated genotypes, and number of VVs analyzed for each condition is given above each bar. *, P < 0.05; **, P < 0.005; χ 2 /Fisher’s exact test. (G) A tiled TEM image of the junction between two adjacent, free-edge cells at P0, shown at lower magnification in Fig. S3 K. n = 3. Bars: 100 nm; 10 nm in inset.

Article Snippet: Antibodies were raised in rabbits to Cx43 (3512; Cell Signaling Technology), sheep to FOXC2 (AF5044; R&D Systems), Foxc2 (AF6989; R&D Systems), and goat to Integrinα9 (BAF3827; R&D Systems).

Techniques: Expressing

Journal: The Journal of Experimental Medicine

Article Title: Human venous valve disease caused by mutations in FOXC2 and GJC2

doi: 10.1084/jem.20160875

Figure Lengend Snippet: Maturation of leaflets and commissures. (A) Immunolocalization at P6 of Nfatc1 (green) and Prox1 (red) in VV of WT mice administered control solvent or cyclosporin ( n = 5 versus 8 VVs, P < 0.05, χ 2 ). (B) Immunolocalization of Foxc2 (green) and Prox1 (red) in VVs of mice of the indicated genotypes. n ≥ 6 per condition. (C and D) Quantification of leaflet length and stage of VV development in mice of the indicated genotypes. Error bars represent means ± SEM. t test for leaflet length. (C, D, G, H, and I) Colors represent developmental stage (see key). The number of VVs analyzed for each condition is given above each bar. *, P < 0.05; **, P < 0.005 (χ 2 for developmental stage). (E) Immunolocalization of Cx37 (arrowheads) and Cx43 in VV leaflets at P6. n ≥ 4. (F) Localization of Prox1, Foxc2, and SMA at P6 in Gja4 −/− vein. n ≥ 6 (G and H) Stages of VV development reached in mice of the indicated genotypes. (I) Localization of Prox1, GFP, and SMA in Gjc2 GFP/GFP KO reporter vein at P2 ( n = 4), and stages of VV development reached in mice of the indicated genotypes. (J) Localization of Cx47-expressing VV cells (arrowheads) of Gjc2 GFP/+ reporter mice at P6. n = 4. Multichannel images are reproduced in supplementary data. Bars, 20 µm. (A–J) Blue stain is PECAM1.

Article Snippet: Antibodies were raised in rabbits to Cx43 (3512; Cell Signaling Technology), sheep to FOXC2 (AF5044; R&D Systems), Foxc2 (AF6989; R&D Systems), and goat to Integrinα9 (BAF3827; R&D Systems).

Techniques: Control, Solvent, Expressing, Staining

Journal: Cell Systems

Article Title: Statistically derived geometrical landscapes capture principles of decision-making dynamics during cell fate transitions

doi: 10.1016/j.cels.2021.08.013

Figure Lengend Snippet: Single-cell resolution analysis of the directed differentiation of ES cells to neural and mesodermal identities (A) Schematic of mESC differentiation. Embryonic stem cells differentiated in defined FGF and WNT signaling regimes adopt either anterior neural (AN), posterior neural (PN), or paraxial mesoderm (M) progenitor identities. Colored bars show the times at which cells were exposed to CHIR and/or FGF. The expected dominant cell type at day 5 and associated marker protein expression is given on the right. CHIR, CHIRON99021; D, day. (B) Representative immunofluorescence images of markers used to identify the different cell types. Progenitors differentiated for 2 days in FGF co-express the early epiblast markers SOX2 and OTX2 (Ba) and adopt SOX1+ OTX2+ AN identity by day 4 (D4) following withdrawal of FGF (Bb). Activation of WNT signaling at D2 with CHIR results in the upregulation of the posterior marker CDX2 (Bc) and the downregulation of OTX2 (Bd) by (D3). Subsequent removal of CHIR at D3 leads to differentiation of SOX1+/CDX2+ PN progenitors (Be), while sustained WNT signaling results in differentiation to TBX6+ early and FOXC2+ late paraxial mesoderm progenitors. (C) Flow-cytometry data. Flow-cytometry analysis of individual progenitors shows the progression from TBX6+ early paraxial mesoderm identity at D4 to FOXC2+ late paraxial mesoderm identity at D5 (Ca) under the sustained WNT signaling regime. At D4, OTX2 and SOX2 remain expressed at high levels in AN progenitors differentiated in the absence of CHIR and are both reduced in PN progenitors induced by transient CHIR, whereas SOX1 expression is highest in PN progenitors (Cb).

Article Snippet: Primary antibodies used: SOX2 (Mouse, Santa Cruz sc-365823), OTX2 (Goat, R&D AF1979), CDX2 (Rabbit, Abcam ab76541), TBX6 (Goat, R&D AF4744), FOXC2 (Sheep, R&D AF6989).

Techniques: Marker, Expressing, Immunofluorescence, Activation Assay, Flow Cytometry

Journal: Cell Systems

Article Title: Statistically derived geometrical landscapes capture principles of decision-making dynamics during cell fate transitions

doi: 10.1016/j.cels.2021.08.013

Figure Lengend Snippet:

Article Snippet: Primary antibodies used: SOX2 (Mouse, Santa Cruz sc-365823), OTX2 (Goat, R&D AF1979), CDX2 (Rabbit, Abcam ab76541), TBX6 (Goat, R&D AF4744), FOXC2 (Sheep, R&D AF6989).

Techniques: Recombinant, Software, Flow Cytometry