Journal: Cancer cell international

Article Title: Cancer-secreted exosomal miR-1825 induces angiogenesis to promote colorectal cancer metastasis.

doi: 10.1186/s12935-025-03674-5

Figure Lengend Snippet: Fig. 6 Schematic diagram showing the mechanism whereby CRC-secreted miR-1825 promotes angiogenesis by downregulating ING1 and activating the TGF-β/Smad2/Smad3 signaling pathway

Article Snippet: The following primary antibodies were used: CD63 (1:1000 dilution, ABclonal, Cat# A5271), TSG101 (1:1000 dilution, Immunoway, Cat# YT4760), ING1 (1:1000 dilution, ABclonal, Cat# A7904), TGF-β (1:1000 dilution, Affinity, Cat# AF1027), Smad2 (1:1000 dilution, Cell Signaling Technology, Cat# 5339), p-Smad2 (1:1000 dilution, Cell Signaling Technology, Cat# 18338), Smad3 (1:1000 dilution, Cell Signaling Technology, Cat# 9513), p-Smad3 (1:1000 dilution, Cell Signaling Technology, Cat# 9520), GAPDH (1:2000, Proteintech, Cat# 10494-1-AP). (See figure on next page.)

Techniques:

Journal: JCI Insight

Article Title: TGF- β promotes fibrosis after severe acute kidney injury by enhancing renal macrophage infiltration

doi: 10.1172/jci.insight.123563

Figure Lengend Snippet: Peritoneal macrophages from Tgfbr2fl/fl (WT) and LysM-Cre Tgfbr2fl/fl (macrophage TGF-βRII–/–; MφTGF-βRII–/–) mice 3 days after peritoneal thioglycollate administration were used. (A) TGF-βRII levels were markedly lower in TGF-βRII–/– macrophages than in WT macrophages. ***P < 0.001, n = 3 in each group. Data were expressed as mean ± SEM. (B) Macrophages were stimulated with 2 ng/ml recombinant TGF-β for 30 minutes. TGF-βRII deletion led to decreases in TGF-β–stimulated phosphorylation of Smad2 and Smad3, an indication of TGF-βRII deficiency. p-Smad3, phospho-Smad3; p-Smad2, phospho-Smad2; FAK, focal adhesion kinase.

Article Snippet: Rat anti-mouse F4/80 (MCA497R, a marker of macrophages) and CD3 (MCA1477, a marker of T lymphocytes) were purchased from AbD Serotec (now Bio-Rad); mouse anti–mannose receptor (CD206, MAB25341) and mouse anti–4-HNE (a marker of oxidative stress, 198960) were from R&D Systems; rabbit anti–TGF-βRII (SC-400) and goat anti-human CTGF (SC-14939) were from Santa Cruz Biotechnology; rabbit anti-human Smad2 (600-401-A59), phospho-Smad2 (600-401-K09S), and phospho-Smad3 (600-401-919) as well as rabbit anti-murine collagen type I (600-401-103-01) were from Rockland Immunochemicals; mouse anti–α-SMA (A5228, a marker of myofibroblasts) was from Sigma-Aldrich; and rabbit anti–TGF-β1 (NBP1-80289) and mouse anti–TGF-β2 (Mab612-SP) were from Novus Biologicals.

Techniques: Recombinant

Journal: Cell Cycle

Article Title: Circ_0008450 downregulates Runx3 to promote the proliferation and epithelial-mesenchymal transition of human keratinized epithelial cells

doi: 10.1080/15384101.2020.1842665

Figure Lengend Snippet: Circ_0008450 silence repressed the TGF-β/Smad signal pathway via the up-regulation of Runx3. (a and b) Keratinized epithelial cells treated with LY2109761 were applied for the detection of phosphorylation of Smads (Smad2 and Smad3) by Western blot. *** p < 0.001. (c and d) Keratinized epithelial cells treated with LY2109761, sh-circ_0008450 (sh-circ_0008450), sh-Runx3 (sh-Runx3) or TGF-β1 were applied for the detection of phosphorylation of Smads (Smad2 and Smad3) by western blot. * p < 0.05, ** p < 0.01 or *** p < 0.001

Article Snippet: Primary antibodies included CyclinD1 (orb77046, Biorbyt), CDK4 (orb225521), cleaved caspase-3 (orb106556), cleaved caspase-9 (orb129033), E-cadherin (orb378741), Vimentin (orb379309), Fibronectin (orb95640), ZO-1 (orb35080), Runx3 (orb153370), p-Smad2 (phospho-S467, orb304593), t-Smad2 (orb99462), p-Smad3 (phospho-S204, orb214215), t-Smad3 (orb304596), and β-actin (orb181785).

Techniques: Western Blot