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Cell Signaling Technology Inc
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Danaher Inc
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Danaher Inc
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GeneTex
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GeneTex
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Thermo Fisher
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Cell Signaling Technology Inc
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Santa Cruz Biotechnology
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Cell Signaling Technology Inc
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GeneTex
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Journal: iScience
Article Title: Cocaine and habit training cause dendritic spine rearrangement in the prelimbic cortex
doi: 10.1016/j.isci.2023.106240
Figure Lengend Snippet: Antibodies used in this report
Article Snippet:
Techniques: Concentration Assay, Sequencing
Journal: iScience
Article Title: Cocaine and habit training cause dendritic spine rearrangement in the prelimbic cortex
doi: 10.1016/j.isci.2023.106240
Figure Lengend Snippet:
Article Snippet:
Techniques: Virus, Plasmid Preparation, Recombinant, Software
Journal: PLoS ONE
Article Title: The Effect of Antenatal Depression and Selective Serotonin Reuptake Inhibitor Treatment on Nerve Growth Factor Signaling in Human Placenta
doi: 10.1371/journal.pone.0116459
Figure Lengend Snippet: Clonality, host species and dilutions of antibodies used in Western blot analysis and immunohistochemistry.
Article Snippet: Also primary antibodies against TrkA (catalogue no 06-574, Upstate, Merck Millipore, US) and
Techniques: Western Blot, Immunohistochemistry
Journal: PLoS ONE
Article Title: The Effect of Antenatal Depression and Selective Serotonin Reuptake Inhibitor Treatment on Nerve Growth Factor Signaling in Human Placenta
doi: 10.1371/journal.pone.0116459
Figure Lengend Snippet: Placental protein levels detected by Western blot.
Article Snippet: Also primary antibodies against TrkA (catalogue no 06-574, Upstate, Merck Millipore, US) and
Techniques: Western Blot
Journal: PLoS ONE
Article Title: The Effect of Antenatal Depression and Selective Serotonin Reuptake Inhibitor Treatment on Nerve Growth Factor Signaling in Human Placenta
doi: 10.1371/journal.pone.0116459
Figure Lengend Snippet: Placental sections stained for NGF, phosphorylated Raf-1 (pRaf-1) and ROCK2 in A) Trophoblasts, B) Endothelial cells and C) Stromal cells.
Article Snippet: Also primary antibodies against TrkA (catalogue no 06-574, Upstate, Merck Millipore, US) and
Techniques: Staining
Journal: Acta Pharmaceutica Sinica. B
Article Title: TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner
doi: 10.1016/j.apsb.2021.04.013
Figure Lengend Snippet: Effects of TMEM16A on the activation of RhoA/ROCK2 signaling pathway induced by AngII in mice BASMCs. (A)–(D) TMEM16A overexpression ameliorated, whereas TMEM16A knockdown promoted, AngII-induced RhoA activation in BASMCs ( n = 5 for each group; ∗ P < 0.05 vs . Con, # P < 0.05 vs . AngII-treated group, one-way ANOVA). (E)–(H) TMEM16A overexpression ameliorated, whereas TMEM16A knockdown promoted, AngII-induced phosphorylation of ROCK2 at Ser 1366 site in BASMCs ( n = 6 for each group; ∗ P < 0.05 vs . Con, # P < 0.05 vs . AngII-treated group, one-way ANOVA). (I) Representative Western blot images of MYPT1 and MLC20 phosphorylation in ROCK2 siRNA and TMEM16A siRNA co-transfected BASMCs. (J) and (K) AngII-induced phosphorylation of MYPT1 at Thr696 site (J) and MLC20 (K) in TMEM16A knockdown BASMCs was abolished by ROCK2 silencing ( n = 6 for each group, ∗ P < 0.05 vs . Con, # P < 0.05 vs . AngII-treated control groups, & P < 0.05 vs . AngII+TM-siRNA group, one-way ANOVA). (L) and (M) AngII-induced cell migration in TMEM16A knockdown BASMCs was inhibited by ROCK2 deletion. Representative images of Transwell assay and statistical analysis were shown ( n = 5 for each group, ∗ P < 0.05 vs . Con, # P < 0.05 vs . TMEM-siRNA group, one-way ANOVA). Values are mean ± SEM.
Article Snippet: Antibodies to
Techniques: Activation Assay, Over Expression, Knockdown, Phospho-proteomics, Western Blot, Transfection, Control, Migration, Transwell Assay
Journal: Acta Pharmaceutica Sinica. B
Article Title: TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner
doi: 10.1016/j.apsb.2021.04.013
Figure Lengend Snippet: TMEM16A inhibited ROCK2 and FAK activation by decreasing WNK1 phosphorylation in BASMCs. (A) and (B) The effect of TMEM16A on AngII (67 nmol/L, 2 min)-induced WNK1 activation. Overexpression of TMEM16A downregulated the increase in AngII-induced WNK1 phosphorylation ( n = 6, ∗ P < 0.05 vs . Con, # P < 0.05 vs . AngII). (C)–(D) The effect of WNK1 on AngII-induced ROCK2 activation. Silencing of WNK1 downregulated AngII-induced increase in the phosphorylation of ROCK2 ( n = 6, ∗ P < 0.05 vs. Con, # P < 0.05 vs . AngII). (E)–(F) The effect of WNK1 on AngII-induced FAK activation. Silencing of WNK1 downregulated AngII-induced increase in the phosphorylation of FAK ( n = 6, ∗ P < 0.05 vs . Con, # P < 0.05 vs . AngII). Values are mean ± SEM.
Article Snippet: Antibodies to
Techniques: Activation Assay, Phospho-proteomics, Over Expression
Journal: Acta Pharmaceutica Sinica. B
Article Title: TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner
doi: 10.1016/j.apsb.2021.04.013
Figure Lengend Snippet: Schematic overview of vascular smooth muscle cell migration regulated by TMEM16A. By suppressing WNK1 activation, TMEM16A inhibited AngII-induced BASMCs migration and vascular remodeling via the RhoA/ROCK2/MLCP/MLC20 and integrin β 3/FAK signaling pathways.
Article Snippet: Antibodies to
Techniques: Migration, Activation Assay, Protein-Protein interactions