Journal: Channels

Article Title: Association of the chemerin-CMKLR1 with atrial potassium current dysregulation and atrial fibrillation in obese mice

doi: 10.1080/19336950.2025.2611704

Figure Lengend Snippet: Localization and expression of potassium channel-associated proteins in mouse atrial myocytes. A. Immunofluorescence images showing membrane localization and expression of Kv4.3, Kv4.2, KChIP2, Kv1.5, and Kir2.1 in atrial cardiomyocytes from LFD and HFD groups. Scale bar, 100 μm. B. Representative Western blotting images and densitometric quantification of Kv4.3, Kv4.2, KChIP2, Kv1.5, and Kir2.1 protein expression in atrial cardiomyocytes from LFD and HFD mice. LFD, low-fat diet; HFD, high-fat diet. Data are presented as mean ± SD ( n = 3). ns, not significant; * p < 0.05, ** p < 0.01 vs. LFD group.

Article Snippet: Primary antibodies diluted in blocking buffer were applied overnight at 4°C as follows: resistin (1:1,000; Abcam, USA), chemerin (1:1,000; Abcam, USA), leptin (1:1,000; Abcam, USA), CMKLR1 (1:1,000; InvitrogenTM, USA), Kv4.3 (1:1,000; Alomone Labs, Israel), Kv4.2 (1:1,000; Alomone Labs, Israel), KChIP2 (1:1,000; Alomone Labs, Israel), Kv1.5 (1:1,000; Alomone Labs, Israel), Kir2.1 (1:1,000; Alomone Labs, Israel), β-Tubulin (1:1,000; Abcam, USA).

Techniques: Expressing, Immunofluorescence, Membrane, Western Blot

Journal: Nature Communications

Article Title: A non-canonical pathway regulates ER stress signaling and blocks ER stress-induced apoptosis and heart failure

doi: 10.1038/s41467-017-00171-w

Figure Lengend Snippet: Mechanism for AGGF1 regulation of miR-183-5p expression. a ChIP–qPCR analysis for the interaction between ZEB1 and miR-183-5p promoter DNA ( n = 4/group, ** P < 0.01). b Schematic diagram showing that the miR-183-5p promoter-luciferase reporter with two ZEB1-binding motifs. c Luciferase activity ( n = 6/group, ** P < 0.01). d Real-time RT-PCR analysis for miR-183-5p expression in H9C2 cells after AGGF1 treatment with or without ZEB1 overexpression ( n = 3/group, ** P < 0.01). e Western blot analysis for the ZEB1 level in H9C2 cells after AGGF1 treatment ( n = 5/group, * P < 0.05). f Western blot analysis for activation of ERK1/2 in H9C2 cells after AGGF1 treatment ( n = 5/group, ** P < 0.01). g Real-time RT-PCR analysis for ERK1 and ERK2 expression by ERK siRNA ( n = 3/group, ** P < 0.01). h Western blot analysis for the ZEB1 level by ERK siRNA ( n = 5/group, * P < 0.05). i Schematic model for a non-canonical ER stress signaling pathway mediated by AGGF1. Data are shown as the mean ± s.d. from at least three independent experiments. Statistical analysis was carried out by a Student’s two-tailed t -test

Article Snippet: Protein–DNA complexes were immunoprecipitated with IgG or an anti-ZEB1 antibody (2 μg; Proteintech).

Techniques: Expressing, ChIP-qPCR, Luciferase, Binding Assay, Activity Assay, Quantitative RT-PCR, Over Expression, Western Blot, Activation Assay, Two Tailed Test

Journal: Cellular signalling

Article Title: SH2D4A inhibits esophageal squamous cell carcinoma progression through FAK/PI3K/AKT signaling pathway.

doi: 10.1016/j.cellsig.2023.110997

Figure Lengend Snippet: Fig. 1. SH2D4A was downregulated in ESCC and lower expression of SH2D4A resulted in an adverse clinical outcome. (A) The mRNA expression of SH2D4A was reduced in GSE53625. (B) The mRNA expression of SH2D4A was reduced in 16 pairs of ESCC tissues detected by RT-qPCR. (C) The expression of SH2D4A were downregulated in ESCC tissues. (D) The relative mRNA expression of SH2D4A was reduced in esophageal carcinoma cell lines detected by RT-qPCR (n = 3 per group). (E) The expression of SH2D4A were downregulated in esophageal carcinoma cell lines. (F, G) Kaplan-Meier analysis of DFS and OS in patients diagnosed with ESCC. All data were provided as mean ± SD. * P < 0.05, and *** P < 0.001.

Article Snippet: Primary antibodies against SH2D4A (15957–1-AP, 1:1000) were purchased from Proteintech.

Techniques: Expressing, Quantitative RT-PCR

Journal: Cellular signalling

Article Title: SH2D4A inhibits esophageal squamous cell carcinoma progression through FAK/PI3K/AKT signaling pathway.

doi: 10.1016/j.cellsig.2023.110997

Figure Lengend Snippet: Fig. 2. SH2D4A overexpression was correlated with a reduction of the proliferation and migration in esophageal carcinoma cells. (A, B) The efficiency of SH2D4A overexpression conducted by lentivirus infection in KYSE-150 and TE-10 (n = 3 per group). (C, D, E) CCK-8 assay, colony formation assay and EDU revealed that SH2D4A overexpression reduce the ability of cells to proliferate (n = 3 per group). (F, G) Transwell migration assay and wound healing assay revealed that SH2D4A overexpression reduce the ability of cells to migrate (n = 3 per group). Scale bar = 100 μm. All data were provided as mean ± SD. * P < 0.05, ** P < 0.01 and *** P < 0.001.

Article Snippet: Primary antibodies against SH2D4A (15957–1-AP, 1:1000) were purchased from Proteintech.

Techniques: Over Expression, Migration, Infection, CCK-8 Assay, Colony Assay, Transwell Migration Assay, Wound Healing Assay

Journal: Cellular signalling

Article Title: SH2D4A inhibits esophageal squamous cell carcinoma progression through FAK/PI3K/AKT signaling pathway.

doi: 10.1016/j.cellsig.2023.110997

Figure Lengend Snippet: Fig. 3. SH2D4 A knockdown promoted the proliferation and migration of esophageal carcinoma cells. (A, B) The efficiency of SH2D4 A knockdown conducted by lentivirus infection in Eca109 and TE-1 (n = 3 per group). (C, D, E) CCK-8 assay, colony formation assay and EDU revealed that SH2D4A knockdown enhance the ability of cells to proliferate (n = 3 per group). (F, G) Transwell migration assay and wound healing assay revealed that SH2D4A knockdown enhance the ability of cells to migrate (n = 3, per group). Scale bar = 100 μm. All data were provided as mean ± SD. * P < 0.05, ** P < 0.01 and *** P < 0.001.

Article Snippet: Primary antibodies against SH2D4A (15957–1-AP, 1:1000) were purchased from Proteintech.

Techniques: Knockdown, Migration, Infection, CCK-8 Assay, Colony Assay, Transwell Migration Assay, Wound Healing Assay

Journal: Cellular signalling

Article Title: SH2D4A inhibits esophageal squamous cell carcinoma progression through FAK/PI3K/AKT signaling pathway.

doi: 10.1016/j.cellsig.2023.110997

Figure Lengend Snippet: Fig. 4. SH2D4A regulated FAK/PI3K/AKT signaling pathway in esophageal cancer cells. (A) SH2D4A was enriched in focal adhesion assemblies through KEGG pathway analysis. (B) Correlation analysis between SH2D4A and related molecules in FAK/PI3K/AKT signaling pathway signaling pathway. (C, D) Expression of FAK/PI3K/AKT signaling pathway-related proteins were determined in different cell lines by western blot.

Article Snippet: Primary antibodies against SH2D4A (15957–1-AP, 1:1000) were purchased from Proteintech.

Techniques: Expressing, Western Blot

Journal: Cellular signalling

Article Title: SH2D4A inhibits esophageal squamous cell carcinoma progression through FAK/PI3K/AKT signaling pathway.

doi: 10.1016/j.cellsig.2023.110997

Figure Lengend Snippet: Fig. 5. SH2D4A inhibited esophageal carcinoma cells from proliferating and migrating through the FAK/PI3K/AKT signaling pathway. (A, B, C) CCK-8 assay, colony formation assay and EDU indicated that PF562271 reduced cell proliferation caused by SH2D4A knockdown (n = 3 per group). (D, E) Transwell migration assay and wound healing assay indicated that PF562271 reduced cell migration caused by SH2D4A knockdown (n = 3 per group). (F) PF562271 reduced the facilitation of FAK/PI3K/AKT signaling pathway caused by SH2D4A knockdown. Scale bar = 100 μm. All data were provided as mean ± SD. * P < 0.05, ** P < 0.01 and *** P < 0.001.

Article Snippet: Primary antibodies against SH2D4A (15957–1-AP, 1:1000) were purchased from Proteintech.

Techniques: CCK-8 Assay, Colony Assay, Knockdown, Transwell Migration Assay, Wound Healing Assay, Migration

Journal: Cellular signalling

Article Title: SH2D4A inhibits esophageal squamous cell carcinoma progression through FAK/PI3K/AKT signaling pathway.

doi: 10.1016/j.cellsig.2023.110997

Figure Lengend Snippet: Fig. 6. SH2D4A knockdown promoted ESCC tumorigenesis in vivo. (A) Tumor sizes were bigger in the si-SH2D4A group than in the si-NC group (n = 5 mice). (B) Growth rate was more rapid in the si-SH2D4A group than in the si-NC group (n = 5 mice). (C) Tumors are heavier in the si-SH2D4A group than in the si-NC group (n = 5 mice). (D) Expression of Ki67 and SH2D4A in tumor tissues were measured by immunohistochemistry. All data were provided as mean ± SD. ** P < 0.01.

Article Snippet: Primary antibodies against SH2D4A (15957–1-AP, 1:1000) were purchased from Proteintech.

Techniques: Knockdown, In Vivo, Expressing, Immunohistochemistry