Journal: Translational Oncology

Article Title: The CHPT-pSTAT3-SLC7A11 signaling axis controls progression and ferroptosis susceptibility of pancreatic cancer

doi: 10.1016/j.tranon.2025.102624

Figure Lengend Snippet: CHPT1 may regulate SLC7A11 transcription by phosphorylating STAT3. A. The results of protein profiling after immunoprecipitation performed by CHPT1 were intersected with the list of transcription factors predicted for SLC7A11 taken to find STAT3. B. Immunoprecipitation (Co-IP) assay to verify the direct interaction of CHPT1 with STAT3. C-D Representative images of immunofluorescence staining showing the colocalization of CHPT1 (red) and STAT3 (green) in PDAC cells. DAPI: blue, nucleus. Line chart of fluorescence signal positioning analysis. E. Protein expression levels of phosphorylated Y705 STAT3 after knockdown and overexpression of CHPT1. F. Protein expression levels of SLC7A11 after treatment with Stattic, an inhibitor of phosphorylated STAT3-Y705 to knockdown CHPT1 cells(5μM and 10μM). G. Co-IP assay confirmed the physical binding of PTPN1 to STAT3. H. CHPT1 overexpression promotes the binding of PTPN1 to STAT3. IP was performed under WB quantification and the differences were significant. I. Immunocytofluorescence analysis showed that overexpression of CHPT1 inhibited the nuclear translocation of pSTAT3.

Article Snippet: After clearing non-specific binding proteins with protein A/G-agarose beads (Selleck, USA), cell lysates were incubated with primary antibodies against CHPT1 (1:100, Santa), STAT3 (1:100, Proteintech), PTPN1(1:100, Proteintech), and IgG control (1:100, Proteintech) overnight at 4°C.

Techniques: Immunoprecipitation, Co-Immunoprecipitation Assay, Immunofluorescence, Staining, Fluorescence, Expressing, Knockdown, Over Expression, Binding Assay, Translocation Assay

Journal: Translational Oncology

Article Title: The CHPT-pSTAT3-SLC7A11 signaling axis controls progression and ferroptosis susceptibility of pancreatic cancer

doi: 10.1016/j.tranon.2025.102624

Figure Lengend Snippet: PTPN1 is the critical effector of CHPT1 in suppressing STAT3-driven PDAC progression. A. Western blot analysis confirming efficient knockdown of PTPN1 in CHPT1-overexpressing PDAC cells. B-D. EDU incorporation assays showing that PTPN1 depletion restores cell proliferation despite CHPT1 overexpression. C. CCK-8 assays demonstrating that PTPN1 knockdown rescues the proliferative capacity of CHPT1-overexpressing cells. E. Transwell migration assays revealing the restoration of migratory potential upon PTPN1 silencing in CHPT1-overexpressing cells. F. Wound healing assays further confirming that PTPN1 depletion reverses the anti-migratory effects of CHPT1 overexpression. All data are presented as mean ± SD from 3 independent experiments (n=3).

Article Snippet: After clearing non-specific binding proteins with protein A/G-agarose beads (Selleck, USA), cell lysates were incubated with primary antibodies against CHPT1 (1:100, Santa), STAT3 (1:100, Proteintech), PTPN1(1:100, Proteintech), and IgG control (1:100, Proteintech) overnight at 4°C.

Techniques: Western Blot, Knockdown, Over Expression, CCK-8 Assay, Migration

Journal: Journal of Enzyme Inhibition and Medicinal Chemistry

Article Title: Identification of novel PTP1B inhibitor for the treatment of LPS-induced myocardial apoptosis: machine learning based virtual screening and biological evaluation

doi: 10.1080/14756366.2025.2596950

Figure Lengend Snippet: PTP1B crystal cluster and inhibitor database analysis. A. The clustering results of collected PTP1B crystals (The PTP1B was divided into 10 clusters and the representative protein was shown in green); B. Chemical space analysis of the training set (yellow) and the test set (red) by principle component analysis.

Article Snippet: The primary antibody PTP1B (Rabbit, dilution: 1: 2000, RRID number: AB_10642566, Cat. NO.: 11334–1-AP) and TCPTP (Rabbit, dilution: 1: 500, RRID number: AB_2173235, Cat. NO.: 11214–1-AP) were purchased from Proteintech.

Techniques:

Journal: Journal of Enzyme Inhibition and Medicinal Chemistry

Article Title: Identification of novel PTP1B inhibitor for the treatment of LPS-induced myocardial apoptosis: machine learning based virtual screening and biological evaluation

doi: 10.1080/14756366.2025.2596950

Figure Lengend Snippet: Pharmacophores produced by selected PTP1B crystal (Green: hydrogen bond acceptor; light blue: Hydrophobic group; dark blue: Hydrophobic group; yellow: Hydrogen bond donor; orange: Aromatic ring; gray: steric hindrance).

Article Snippet: The primary antibody PTP1B (Rabbit, dilution: 1: 2000, RRID number: AB_10642566, Cat. NO.: 11334–1-AP) and TCPTP (Rabbit, dilution: 1: 500, RRID number: AB_2173235, Cat. NO.: 11214–1-AP) were purchased from Proteintech.

Techniques: Produced

Journal: Journal of Enzyme Inhibition and Medicinal Chemistry

Article Title: Identification of novel PTP1B inhibitor for the treatment of LPS-induced myocardial apoptosis: machine learning based virtual screening and biological evaluation

doi: 10.1080/14756366.2025.2596950

Figure Lengend Snippet: The structures, activities and binding modes of selected compounds. A. The structures of selected compounds through virtual screening; B. PTP1B inhibitory rate of selected compounds at the concentration of 20 μM; C. The IC 50 value of PI-2 against PTP1B; D. The binding modes of PI-2 with PTP1B through molecular docking.

Article Snippet: The primary antibody PTP1B (Rabbit, dilution: 1: 2000, RRID number: AB_10642566, Cat. NO.: 11334–1-AP) and TCPTP (Rabbit, dilution: 1: 500, RRID number: AB_2173235, Cat. NO.: 11214–1-AP) were purchased from Proteintech.

Techniques: Binding Assay, Concentration Assay

Journal: Journal of Enzyme Inhibition and Medicinal Chemistry

Article Title: Identification of novel PTP1B inhibitor for the treatment of LPS-induced myocardial apoptosis: machine learning based virtual screening and biological evaluation

doi: 10.1080/14756366.2025.2596950

Figure Lengend Snippet: The PTP1B inhibitory selectivity of PI-2 at the enzymatic and the cellular level. A. The IC 50 value of PI-2 against TCPTP; B. The IC 50 value of PI-2 against ACP1; C-E. The effect of PI-2 on the stability of PTP1B and TCPTP in AC16 cells.

Article Snippet: The primary antibody PTP1B (Rabbit, dilution: 1: 2000, RRID number: AB_10642566, Cat. NO.: 11334–1-AP) and TCPTP (Rabbit, dilution: 1: 500, RRID number: AB_2173235, Cat. NO.: 11214–1-AP) were purchased from Proteintech.

Techniques:

Journal: Journal of Enzyme Inhibition and Medicinal Chemistry

Article Title: Identification of novel PTP1B inhibitor for the treatment of LPS-induced myocardial apoptosis: machine learning based virtual screening and biological evaluation

doi: 10.1080/14756366.2025.2596950

Figure Lengend Snippet: The effect of PI-2 on mitochondrial membrane potential through PTP1B/JNK pathway. A. The effect of PI-2 on the phosphorylation level of JNK; B. The effect of PI-2 on mitochondrial membrane potential.

Article Snippet: The primary antibody PTP1B (Rabbit, dilution: 1: 2000, RRID number: AB_10642566, Cat. NO.: 11334–1-AP) and TCPTP (Rabbit, dilution: 1: 500, RRID number: AB_2173235, Cat. NO.: 11214–1-AP) were purchased from Proteintech.

Techniques: Membrane, Phospho-proteomics

Journal: Molecular Neurobiology

Article Title: Metformin Ameliorates Early Brain Injury After Subarachnoid Hemorrhage Via Improving Endoplasmic Reticulum Stress and Mitochondrial Stress-Mediated Ca 2+ Imbalance

doi: 10.1007/s12035-025-05558-1

Figure Lengend Snippet: Severity of ERS, MS, and Ca2 + imbalance in the initial 72 h following SAH in the temporal cortex of mice in vivo. A – C Representative Western blot band and densitometric quantification of the time-dependent expression of CHOP and ATF4 in the temporal cortex of SAH mice models in the initial 72 h. ns P > 0.05, * P < 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). Samples derived from the same experiment, and the gels were processed in parallel. Protein expression levels were normalized to GAPDH as an internal control. Individual gels were run for the separate proteins when the loading protein amount was consistent. D The arterial blood glucose in the SAH model groups. ns P > 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). E – L Representative Western blot band and densitometric quantification of the time-dependent expression of PTP1B, p-AKT, AKTp-eIF2a, eIF2a, Bcl-2, Bax, and CC3 in the temporal cortex of SAH mice models in the initial 72 h. ns P > 0.05, * P < 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). M The concentration of Ca 2+ in the temporal cortex of SAH groups. ns P > 0.05, * P < 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). N – Q Immunofluorescence revealed the number of TUNEL-positive cells in the initial 72 h following SAH in the bilateral temporal cortex and CA3, N = 4 per group, scale bar = 50 μm. An unpaired Student’s t test was used for comparisons between two groups, whereas ANOVA followed by Tukey’s post hoc test was used for comparisons among multiple groups

Article Snippet: The PVDF membrane was blocked in 5% skim milk for 90 min at room temperature, followed by incubation with the primary antibodies against PTP1B (1:2000 Proteintech, catalog number 11334–1-AP), IP3R1 (1:2000, Abcam, catalog number ab264281), CHOP (1:1000, Proteintech, catalog number 15204–1-AP), Bcl-2 (1:2000, Affinity, lot# 70g9181), Bax (1:2000, Proteintech, catalog number 50599–2-2 g), VDAC1 (1:2000, Proteintech, catalog number 10866–1-AP), AKT (1:1000 Proteintech, catalog number 10176–2-AP), p-AKT (1:1000 Proteintech, catalog number 80455–1-RR), GRP75 (1:1000, Bio-Techne, catalog number MAB3584, ATF4 (1:2000, Proteintech, catalog number 10835–1-AP, p- eIF2a (1:500, Affinity, catalog number AF3087), eIF2a (1:1000, Proteintech, catalog number 11170–1-AP), and CC3 (1:1000, Bioss, Boston, MA, USA lot: BJ03319208), respectively.

Techniques: In Vivo, Western Blot, Expressing, Derivative Assay, Control, Concentration Assay, Immunofluorescence, TUNEL Assay

Journal: Molecular Neurobiology

Article Title: Metformin Ameliorates Early Brain Injury After Subarachnoid Hemorrhage Via Improving Endoplasmic Reticulum Stress and Mitochondrial Stress-Mediated Ca 2+ Imbalance

doi: 10.1007/s12035-025-05558-1

Figure Lengend Snippet: ERSand MS mediated the IP3R1–GRP75–VDAC1 Ca2 + channeling complex in the first 72 h following SAH in the temporal cortex of mice in vivo. A – D Representative Western blot band and densitometric quantification of the time-dependent expression of IP3R1, GRP75, and VDAC1 in the temporal cortex of SAH mice models in the initial 72 h. The expression of the IP3R1–GRP75–VDAC1 complex was upregulated. ns P > 0.05, * P < 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). Samples derived from the same experiment, and the gels were processed in parallel. Protein expression levels were normalized to GAPDH as an internal control. Individual gels were run for the separate proteins when the loading protein amount was consistent. E – F Conventional immunofluorescence of PTP1B, Calnexin, VDAC1, and DAPI in the bilateral temporal cortex and CA3. The subsequent MAM junction variation was detected by the conventional immunofluorescence colocalization of calnexin and VDAC1 in vivo. Scale bar = 50 μm, N = 4 per group. G – I The outline and the proportion of surviving neurons induced by SAH in the bilateral temporal cortex and CA3 region. Scale bar = 50 μm, N = 4 per group. J The TEM showed dilated rough ER fragments and swollen mitochondria in the bilateral temporal cortex in each group. Images were acquired at a magnification of 20,000 × , Scale bar = 250 nm. An unpaired Student’s t test was used for comparisons between two groups, whereas ANOVA followed by Tukey’s post hoc test was used for comparisons among multiple groups

Article Snippet: The PVDF membrane was blocked in 5% skim milk for 90 min at room temperature, followed by incubation with the primary antibodies against PTP1B (1:2000 Proteintech, catalog number 11334–1-AP), IP3R1 (1:2000, Abcam, catalog number ab264281), CHOP (1:1000, Proteintech, catalog number 15204–1-AP), Bcl-2 (1:2000, Affinity, lot# 70g9181), Bax (1:2000, Proteintech, catalog number 50599–2-2 g), VDAC1 (1:2000, Proteintech, catalog number 10866–1-AP), AKT (1:1000 Proteintech, catalog number 10176–2-AP), p-AKT (1:1000 Proteintech, catalog number 80455–1-RR), GRP75 (1:1000, Bio-Techne, catalog number MAB3584, ATF4 (1:2000, Proteintech, catalog number 10835–1-AP, p- eIF2a (1:500, Affinity, catalog number AF3087), eIF2a (1:1000, Proteintech, catalog number 11170–1-AP), and CC3 (1:1000, Bioss, Boston, MA, USA lot: BJ03319208), respectively.

Techniques: In Vivo, Western Blot, Expressing, Derivative Assay, Control, Immunofluorescence

Journal: Molecular Neurobiology

Article Title: Metformin Ameliorates Early Brain Injury After Subarachnoid Hemorrhage Via Improving Endoplasmic Reticulum Stress and Mitochondrial Stress-Mediated Ca 2+ Imbalance

doi: 10.1007/s12035-025-05558-1

Figure Lengend Snippet: Met significantly suppressed Ca2 + transfer from the ER to the mitochondria through the PTP1B/AKT following SAH 24 h in the temporal cortex of mice in vivo. A – G To determine the regulatory role of Met in ER stress and mitochondrial signaling, we employed lentivirus-mediated modulation in a 24-h SAH model and confirmed the effects by Western blot analysis. Representative Western blot band and densitometric quantification of the time-dependent expression of CHOP, ATF4, PTP1B, p-eIF2a, eIF2a, p-AKT, and AKT following SAH 24 h in vivo. ns P > 0.05, * P < 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). Samples derived from the same experiment, and the gels were processed in parallel. Protein expression levels were normalized to GAPDH as an internal control. Individual gels were run for the separate proteins when the loading protein amount was consistent. H The effect of Met on the concentration of Ca 2+ in the temporal cortex of SAH groups. ns P > 0.05, * P < 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). I – L Representative Western blot band and densitometric quantification of the time-dependent expression of IP3R1, GRP75, and VDAC1 in vivo. ns P > 0.05, * P < 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). M , N The effect of Met on the conventional immunofluorescence of PTP1B, calnexin, VDAC1, and DAPI in the bilateral temporal cortex and CA3. The subsequent MAM junction variation was detected by the conventional immunofluorescence colocalization of calnexin and VDAC1 in vivo. Scale bar = 50 μm, N = 4 per group. An unpaired Student’s t test was used for comparisons between two groups, whereas ANOVA followed by Tukey’s post hoc test was used for comparisons among multiple groups

Article Snippet: The PVDF membrane was blocked in 5% skim milk for 90 min at room temperature, followed by incubation with the primary antibodies against PTP1B (1:2000 Proteintech, catalog number 11334–1-AP), IP3R1 (1:2000, Abcam, catalog number ab264281), CHOP (1:1000, Proteintech, catalog number 15204–1-AP), Bcl-2 (1:2000, Affinity, lot# 70g9181), Bax (1:2000, Proteintech, catalog number 50599–2-2 g), VDAC1 (1:2000, Proteintech, catalog number 10866–1-AP), AKT (1:1000 Proteintech, catalog number 10176–2-AP), p-AKT (1:1000 Proteintech, catalog number 80455–1-RR), GRP75 (1:1000, Bio-Techne, catalog number MAB3584, ATF4 (1:2000, Proteintech, catalog number 10835–1-AP, p- eIF2a (1:500, Affinity, catalog number AF3087), eIF2a (1:1000, Proteintech, catalog number 11170–1-AP), and CC3 (1:1000, Bioss, Boston, MA, USA lot: BJ03319208), respectively.

Techniques: In Vivo, Western Blot, Expressing, Derivative Assay, Control, Concentration Assay, Immunofluorescence

Journal: Molecular Neurobiology

Article Title: Metformin Ameliorates Early Brain Injury After Subarachnoid Hemorrhage Via Improving Endoplasmic Reticulum Stress and Mitochondrial Stress-Mediated Ca 2+ Imbalance

doi: 10.1007/s12035-025-05558-1

Figure Lengend Snippet: Met significantly suppressed Ca 2+ transfer from the ER to the mitochondria through the PTP1B/AKT following SAH 24 h in vitro. A – K Our vitro data demonstrate that PTP1B plays a critical role in integrating ER stress with mitochondrial dysfunction following SAH 24 h. Representative Western blot band and densitometric quantification of PTP1B, p-AKT, AKT, p-eIF2a, eIF2a, IP3R1, GRP75, VDAC1, ATF4, and CHOP in primary neurons induced by the OxyHb. The expression of the IP3R1–GRP75–VDAC1 complex was upregulated accordingly. ns P > 0.05, * P < 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). Samples derived from the same experiment, and the gels were processed in parallel. Protein expression levels were normalized to GAPDH as an internal control. Individual gels were run for the separate proteins when the loading protein amount was consistent. L Conventional immunofluorescence confirmed the colocalization of NEUN, MAP-2, and DAPI in primary neurons. Scale bar = 50 μm. M – R The effect of Met on the apoptosis of SAH in vitro. Representative Western blot bands of Bcl-2, Bax, CC3, and flow cytometry were used to evaluate the effect of Met on apoptosis in vivo. ns P > 0.05, * P < 0.05. Values were presented as the mean ± SD from four independent experiments ( N = 4). Protein expression levels were normalized to GAPDH as an internal control. S The conventional immunofluorescence staining showed that the colocalization of intracellular Ca 2+ concentration increased significantly in the OxyHb24H group in primary neurons. Scale bar = 50 μm. T The conventional immunofluorescence confirmed the colocalization of PTP1B, calnexin, VDAC1, and DAPI in primary neurons after the intervention of lentivirus and inhibitors. To assess the effect of Met on MAM integrity, we performed immunofluorescence co-localization analysis of the ER marker calnexin and the mitochondrial marker VDAC1 in treated primary neurons. Scale bar = 50 μm. An unpaired Student’s t test was used for comparisons between two groups, whereas ANOVA followed by Tukey’s post hoc test was used for comparisons among multiple groups

Article Snippet: The PVDF membrane was blocked in 5% skim milk for 90 min at room temperature, followed by incubation with the primary antibodies against PTP1B (1:2000 Proteintech, catalog number 11334–1-AP), IP3R1 (1:2000, Abcam, catalog number ab264281), CHOP (1:1000, Proteintech, catalog number 15204–1-AP), Bcl-2 (1:2000, Affinity, lot# 70g9181), Bax (1:2000, Proteintech, catalog number 50599–2-2 g), VDAC1 (1:2000, Proteintech, catalog number 10866–1-AP), AKT (1:1000 Proteintech, catalog number 10176–2-AP), p-AKT (1:1000 Proteintech, catalog number 80455–1-RR), GRP75 (1:1000, Bio-Techne, catalog number MAB3584, ATF4 (1:2000, Proteintech, catalog number 10835–1-AP, p- eIF2a (1:500, Affinity, catalog number AF3087), eIF2a (1:1000, Proteintech, catalog number 11170–1-AP), and CC3 (1:1000, Bioss, Boston, MA, USA lot: BJ03319208), respectively.

Techniques: In Vitro, Western Blot, Expressing, Derivative Assay, Control, Immunofluorescence, Flow Cytometry, In Vivo, Staining, Concentration Assay, Marker

Journal: Journal of Ginseng Research

Article Title: (20S)-protopanaxatriol attenuates Ang II-induced renal injury via PTPN1-mediated AMPK/mTOR signaling pathway

doi: 10.1016/j.jgr.2025.08.009

Figure Lengend Snippet: The potential target proteins of PPT were determined through network analysis and the effect of PPT on autophagy of renal cells was confirmed (A) In silico prediction of PPT's molecular targets was performed using web-based tools. (B) Molecular docking of PPT with PTPN1. (C) PPT treatment increases protease susceptibility of the PTPN1 in cell lysates as determined by the DARTS assay. (D) NRK-52E cells were treated with 6 μM PPT for 2 h and subsequently heated at different temperatures for 3 min. After freeze-thaw cycles for cell lysis, the soluble PTPN1 protein levels were examined by Western blotting. (E) Western blotting was used to detect the expression of PTPN1 in the renal tissue. GAPDH was included as a loading control. (F) Densitometric quantification of electrophoretic bands from panel E using ImageJ analytical modules. Datasets expressed as mean ± SEM (n = 6 biological replicates). Statistical comparisons performed using two-tailed t -test: ns = non-significant; ∗ p < 0.05, p < 0.01 vs control cohort; # p < 0.05, ## p < 0.01 vs Ang II-treated group.

Article Snippet: Antibodies against PTPN1 (Cat. #11334-1-AP), P62/SQSTM1 (Cat. # 18420-1-AP), Beclin 1 (Cat. # 11306-1-AP), LC3 (Cat. # 14600-1-AP), IκBα (Cat. # 10268-1-AP), p-P65 Ser468 (Cat. # 14600-1-AP) were procured from Proteintech (China). p-AMPKα Thr172 (Cat. #2535), AMPKα (Cat. #2532), p-mTOR Ser2448 (Cat. #5536) and mTOR (Cat. #2983) were procured from Cell Signaling Technology (USA).

Techniques: In Silico, Lysis, Western Blot, Expressing, Control, Two Tailed Test

Journal: Journal of Ginseng Research

Article Title: (20S)-protopanaxatriol attenuates Ang II-induced renal injury via PTPN1-mediated AMPK/mTOR signaling pathway

doi: 10.1016/j.jgr.2025.08.009

Figure Lengend Snippet: PPT reduces Ang II‐induced fibrosis in NRK-52E cells NRK-52E renal tubular epithelial cells underwent a pretreatment protocol with 5 or 10 μM PPT for 1 h prior to Ang II stimulation (1 μM, 8/24 h). (A) Cytocompatibility assessment via colorimetric MTT cell viability assay (n = 3 technical replicates). (B) Immunoblot detection of fibrotic biomarkers COL-IV and TGF-β1 with GAPDH normalization. (C) Densitometric quantification of electrophoretic bands from panel B using ImageJ analytical modules. (D) Quantitative gene expression analysis of Col4 and Tgfb transcripts via RT-qPCR amplification. (E) Western blotting was used to detect the expression of PTPN1 in the NRK-52E cells. GAPDH was included as a loading control. (F) Densitometric quantification of electrophoretic bands from panel E using ImageJ analytical modules. (G – I) Inflammatory cytokine transcript quantification ( Il1b, Il6, Tnf ) in NRK-52E cells by reverse transcription-quantitative PCR. (J) Pharmacological interrogation protocol: NRK-52E cultures received 1 h pretreatment with PPT (5/10 μM) ± PTPN1 inhibitor cocktail (5 μM: Trodusquemine) followed by 2 h Ang II stimulation (1 μM). Subsequent biomolecular extraction facilitated parallel immunoblotting and transcriptional analysis. Representative immunodetection of fibrotic effectors COL-IV and TGF-β1 with GAPDH normalization. (K) Densitometric quantification of panel J immunoblots. (L – N) Inflammatory transcriptome mapping of Il1b, Il6, and Tnf via quantitative reverse transcription PCR. All data expressed as mean ± SEM (n = 3 biological experiments). Statistical significance determined by two-tailed t -test: ∗ p < 0.05, ∗∗ p < 0.01 vs untreated controls; # p < 0.05, ## p < 0.01 vs Ang II-challenged cells.

Article Snippet: Antibodies against PTPN1 (Cat. #11334-1-AP), P62/SQSTM1 (Cat. # 18420-1-AP), Beclin 1 (Cat. # 11306-1-AP), LC3 (Cat. # 14600-1-AP), IκBα (Cat. # 10268-1-AP), p-P65 Ser468 (Cat. # 14600-1-AP) were procured from Proteintech (China). p-AMPKα Thr172 (Cat. #2535), AMPKα (Cat. #2532), p-mTOR Ser2448 (Cat. #5536) and mTOR (Cat. #2983) were procured from Cell Signaling Technology (USA).

Techniques: Viability Assay, Western Blot, Gene Expression, Quantitative RT-PCR, Amplification, Expressing, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Extraction, Immunodetection, Two Tailed Test

Journal: Journal of Ginseng Research

Article Title: (20S)-protopanaxatriol attenuates Ang II-induced renal injury via PTPN1-mediated AMPK/mTOR signaling pathway

doi: 10.1016/j.jgr.2025.08.009

Figure Lengend Snippet: Graphical abstract mechanism of (20S)-Protopanaxatriol in alleviating hypertensive inflammatory kidney injury by targeting the PTPN1-Mediated AMPK/mTOR autophagy signaling pathway.

Article Snippet: Antibodies against PTPN1 (Cat. #11334-1-AP), P62/SQSTM1 (Cat. # 18420-1-AP), Beclin 1 (Cat. # 11306-1-AP), LC3 (Cat. # 14600-1-AP), IκBα (Cat. # 10268-1-AP), p-P65 Ser468 (Cat. # 14600-1-AP) were procured from Proteintech (China). p-AMPKα Thr172 (Cat. #2535), AMPKα (Cat. #2532), p-mTOR Ser2448 (Cat. #5536) and mTOR (Cat. #2983) were procured from Cell Signaling Technology (USA).

Techniques: