traf6  (Cell Signaling Technology Inc)

Journal: iScience

Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway

doi: 10.1016/j.isci.2026.115173

Figure Lengend Snippet: FHL2 interacts with TRAF6 (A) Representative IF images of FHL2 and TRAF6 expression in kidney tissues (Scale bars, 100 μm). (B–C) The expression of TRAF6 and NF-κB pathway-related proteins in HK-2 cell lines after FHL2 overexpression was examined by Western blot. GAPDH was used as a loading control. (D) CoIP experiments validate the interaction between FHL2 and TRAF6. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

Article Snippet: TRAF6 , Affinity Biosciences , Cat# AF5376; RRID: AB_2810280.

Techniques: Expressing, Over Expression, Western Blot, Control

Journal: Neural Regeneration Research

Article Title: Overexpression of the inwardly rectifying potassium channel Kir4.1 or Kir4.1 Tyr 9 Asp in Müller cells exerts neuroprotective effects in an experimental glaucoma model

doi: 10.4103/NRR.NRR-D-24-00461

Figure Lengend Snippet: Kir4.1 overexpression and Kir4.1 Tyr 9 Asp overexpression in Müller cells suppress the MYD88/IRAK1/TRAF6/NF-κB p65 inflammatory signaling pathway. (A) Representative immunoblots showing changes in MYD88, IRAK1, TRAF6, and NF-κB p65 expression levels in microglia co-cultured with normal or activated Müller cells infected with LV-NC, Kir4.1, and Kir4.1 Tyr 9 Asp lentiviruses. (B, D, F, H) Bar charts summarizing the average densitometric quantification of immunoreactive bands for MYD88 (B), IRAK1 (D), TRAF6 (F), and NF-κB p65 (H) in microglia co-cultured with normal or activated Müller cells. n = 5 for each group. * P < 0.05, ** P < 0.01, vs. the + normal Müller cells group. Unpaired two-tailed t -test. (C, E, G, I) Bar charts summarizing the average densitometric quantification of immunoreactive bands for MYD88 (C), IRAK1 (E), TRAF6 (G), and NF-κB p65 (I) in microglia co-cultured with normal or activated Müller cells. n = 5 for each group. * P < 0.05, ** P < 0.01, vs. LV-NC + normal Müller cells group. One-way analysis of variance (Tukey–Kramer multiple comparisons test) was performed. eGFP: Enhanced green fluorescent protein; IRAK1: IL-1 receptor associated kinase 1; LV-NC: eGFP control lentiviruses; MYD88: myeloid differentiation primary response protein 88; NF-κB P65: nuclear factor kappa B P65; TRAF6: TNF receptor associated factor 6.

Article Snippet: Previous studies have demonstrated that Toll-like receptors play a role in microglial activation and the release of pro-inflammatory factors in the COH retina, a process mediated by the MYD88/IRAK1/TRAF6/NF-κB p65 signaling pathway (Takeda and Akira, 2004; Luo et al., 2010; Weber et al., 2010; Miao et al., 2023).

Techniques: Over Expression, Western Blot, Expressing, Cell Culture, Infection, Two Tailed Test, Control