Journal: The Journal of comparative neurology

Article Title: Domain-specific distribution of gap junctions defines cellular coupling to establish a vascular relay in the retina

doi: 10.1002/cne.24699

Figure Lengend Snippet: Primary antibodies

Article Snippet: Connexin 37 , (C)EHQMAKISVAEDGR , rabbit , 1:2000 , poly , Alomone, ACC-204 , RRID:AB_2722598.

Techniques: Marker, Purification, Recombinant

Journal: JCI Insight

Article Title: Mutations in EPHB4 cause human venous valve aplasia

doi: 10.1172/jci.insight.140952

Figure Lengend Snippet: ( A ) Localization of PECAM1 (blue), and either Cx37 or Cx43, as indicated (magenta) around VFCs on P0 in heterozygous Efnb2GFP (green) mice. As expected, on P0 Cx37 was localized to Efnb2GFP-expressing VFCs, primarily forming large gap junction plaques (examples indicated between arrowheads) and Cx43 was localized to endothelium upstream of these VFCs (region to the left of the arrowheads). Smaller plaques are also identifiable. ( B ) Localization of PECAM1 (blue), Prox1 (red), and either Cx37 or Cx43, as indicated (green), after homozygous deletion of Efnb2 . The tightly regulated expression pattern of Cx37 was disrupted, with expression over a wider area (arrowheads) and the typical appearance of larger plaques was lost. The expression pattern of Cx43 was also disrupted and no longer confined to upstream of VFCs (arrowheads; P < 0.05, χ 2 test of the proportion of VVs showing normal [confined] vs. disrupted expression pattern, n ≥ 6 VV per group). ( C and D ) The proportion of proliferating VFCs was assessed by colocalization of Prox1 and Ki67 (arrowheads). Ki67 + VFCs were easily identified in littermate controls, but far fewer proliferating VFCs were identifiable after homozygous Efnb2 deletion. The inferior region of the vein is shown; **** P < 0.00005, unpaired 2-tailed t test, n ≥ 6 VV per group, data are shown as mean ± SEM). Scale bars in A–C : 20 μm. VFCs, valve-forming cells; VVs, venous valves; P0, postnatal day 0.

Article Snippet: The following antibodies were used: rabbit anti-Cx43 (Cell Signaling Technology 3512), Cx37 (CX37A11, Alpha Diagnostics), Prox1 (11-002P, Angiobio), ki67 (ab15580, Abcam), and Golgi apparatus protein 1 (ab103439, Abcam); sheep anti-Foxc2 (AF6989, R&D); goat anti-EphB4 (BAF446, R&D); rat anti-PECAM1 (clone MEC 13.3, BD); and mouse anti-α smooth muscle actin (clone 1A4 conjugated to Cy3, MilliporeSigma).

Techniques: Expressing