anti pchk2 t68  (Cell Signaling Technology Inc)

Journal: bioRxiv

Article Title: miR-378a and NPNT coordinate autophagy regulation in podocytes through mTOR and MAPK signaling

doi: 10.64898/2026.03.19.709781

Figure Lengend Snippet: a-c: Western blot analysis of EGFR (a), AKT (b) and ERK1/2 (c) phosphorylation in podocytes following NPNT siRNA or control siRNA transfection. Phospho-protein levels were normalized to total protein levels, respectively. Vinculin (a) or GAPDH (b, c) served as loading controls. Data is presented as fold change relative to control siRNA (Ctrl). Data represent mean ± SD, n = 3-5 independent experiments. * p <0.05.

Article Snippet: Primary antibodies used in this study: Phospho-Akt (Ser473, #9271S, Cell Signaling), AKT (#9272, Cell Singaling), phospho-EGFR (Tyr1068, #3777S, Cell Signaling), EGFR (#2232, Cell Signaling), phospho-ERK1/2 (phosphor-p44/42 MAPK (Thr202/Tyr204), #9106, Cell Signaling), ERK1/2 (p44/42 MAPK, #9102, Cell Signaling), GAPDH (sc-32233, Santa Cruz), LC3 (NB100-2220, Novus), phospho-mTOR (Ser2448, #5536S, Cell Signaling), mTOR (2983S, Cell Signaling), vinculin (V9131, Sigma-Aldrich).

Techniques: Western Blot, Phospho-proteomics, Control, Transfection

Journal: Cell Death & Disease

Article Title: Declined RTN3 stabilizes DHCR7 to induce cholesterol-dependent tumor progression and MEK inhibitors insensitivity in thyroid cancer

doi: 10.1038/s41419-026-08538-y

Figure Lengend Snippet: A Cholesterol concentrations in KTC-1 (left) and K1 (right) cells with RTN3 knockout, knockdown and overexpression, n = 3. B The effects of cholesterol and its inhibitor Simvastatin on the activation of EGFR/ERK pathway indicated by p-EGFR and p-ERK levels detected by WB assay in KTC-1 (left) and K1 (right) cells. C WB analysis of p-EGFR and p-ERK levels after RTN3 knockout, knockdown and overexpression in KTC-1 (left) and K1 (right) cells. D WB analysis of the effects of Simvastatin treatment on p-EGFR and p-ERK levels in RTN3 knockout cells. E –G Cell proliferation ability determined by CCK-8 assays ( E ) and EdU assays ( F ) with representative images in the left (scale bar, 40 μm) and the quantification of EdU positive cell ratios in the right, and colony-formation assays ( G ), n = 3. H , I Cell migration ability determined by transwell assays ( H ) (scale bar, 40 μm) and wound healing assays ( I ) (scale bar, 100 μm), with representative images in the left and the quantification graphs in the right, n = 3. *: P < 0.05, ***: P < 0.001, ****: P < 0.0001, ns: P ≥ 0.05.

Article Snippet: The following antibodies were used: GAPDH (10494-1-AP, Proteintech), RTN3 (68215-1-Ig, Proteintech), DHCR7 (PA5-48204, Invitrogen), ERK (4695, CST), p-ERK (4376, CST), EGFR (2232, CST), p-EGFR (2234, CST).

Techniques: Knock-Out, Knockdown, Over Expression, Activation Assay, CCK-8 Assay, Migration