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Kir4.1 overexpression and Kir4.1 Tyr 9 Asp overexpression in Müller cells suppress the <t>MYD88/IRAK1/TRAF6/NF-κB</t> <t>p65</t> 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.
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Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) <t>Apoptosis</t> assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.
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Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) <t>Apoptosis</t> assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.
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Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) <t>Apoptosis</t> assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.
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Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) <t>Apoptosis</t> assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.
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Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) <t>Apoptosis</t> assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.
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Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) <t>Apoptosis</t> assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.
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Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) <t>Apoptosis</t> assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.
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Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) <t>Apoptosis</t> assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.
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Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) <t>Apoptosis</t> assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.
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Image Search Results


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.

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

Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) Apoptosis assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.

Journal: Genomics

Article Title: Comprehensive analysis of cuproptosis genes and cuproptosis-related genes as prognosis factors in esophageal squamous cell carcinoma.

doi: 10.1016/j.ygeno.2023.110732

Figure Lengend Snippet: Fig. 10. Inhibitory effect of milciclib to ESCC. (A) CCK8 assay. (B, C) Colony formation assay. (D) Wound healing assay, Scale bar: 100×. (E) Apoptosis assays. (F) Western blotting of FDX1, CDKN2A, and DLD expression in KYSE150 and KYSE510 after milciclib treatment for 48 h. Statistics are presented as the mean ± SEM.

Article Snippet: Next, apoptosis was detected using the Annexin V-FITC apoptosis detection kit (Beyotime, Z. Wu et al. Genomics 115 (2023) 110732 C1062L) according to the manufacturer's instructions.

Techniques: CCK-8 Assay, Colony Assay, Wound Healing Assay, Western Blot, Expressing