Journal: Molecules and Cells

Article Title: Tankyrase-1-mediated PARsylation directs TFEB partner switching to regulate selective Wnt target gene expression

doi: 10.1016/j.mocell.2026.100313

Figure Lengend Snippet: PARsylation of TFEB is crucial for its interaction with TCF-1/LEF-1 and Wnt-TFEB target gene expression. (A) TFEB with mutations at residues 237K and 274K is not PARsylated by TNKS1. (B, C) TFEB with mutations in the PARsylation sites does not bind to HA-TCF-1 (B) or HA-LEF-1 (C) in HEK293T cells. (D) The self-interaction of the TFEB mutant, which has mutations at PARsylation sites, was not reduced by the treatment of Wnt3a-CM. HEK293A cells were transfected with TFEB mutants carrying different tags and treated with Wnt3a-CM for 2 hours. (E) Treatment of HEK293A cells with Wnt3a-CM for 2 hours does not reduce the level of oligomer of TFEB PARsylation-defective mutants. (F) PARsylation of TFEB is necessary for Wnt-TFEB target gene expression. HEK293A cells were knocked down and transfected with the indicated constructs, then treated with Wnt3a-CM for 8 hours. The cells were then used for real-time PCR. Statistical analysis was performed using a 2-tailed unpaired t-test, showing exact P- values in each figure. Error bars indicate the standard deviation of triplicate measurements (technical replicates).

Article Snippet: Quantitative real-time PCR (qPCR) was conducted using THUNDERBIRD SYBR qPCR Mix (Toyobo, QPS-201) in accordance with the manufacturer’s instructions.

Techniques: Targeted Gene Expression, Mutagenesis, Transfection, Construct, Real-time Polymerase Chain Reaction, Standard Deviation

Journal: Redox Biology

Article Title: Triclosan exacerbates post-myocardial infarction injury via Nur77 ubiquitination: Linking NTRK2/PGC-1α-mediated mitochondrial dysfunction to senescence and ferroptosis

doi: 10.1016/j.redox.2026.104022

Figure Lengend Snippet: Long-term exposure to three doses of TCS exacerbated short- and long-term cardiac injury after MI in mice For male mice: (A) Representative echocardiographic images of mouse hearts on day 3 post-surgery, including the sham operation group, vehicle control group (8-week exposure followed by MI surgery), and low-, medium-, and high-dose TCS exposure groups (8-week exposure followed by MI surgery). (B) Quantitative analysis of cardiac function parameters EF% and FS% in the five groups on day 3 post-sham operation (n = 10) or post-MI surgery (n = 12 per group). (C, D) Serum levels of CK-MB and cTnT in the five groups on day 3 post-sham operation or post-MI surgery (n = 8 per group). (E) Representative HE-stained images of mouse hearts from the five groups (Scale bar = 0.5 mm). (F, G) Representative fluorescent images of F4/80 and cTnI co-staining in mouse hearts and quantitative analysis of F4/80 expression across groups (Scale bar = 40 μm, n = 6 per group). (H) Representative Western blots and quantitative analyses of Ly6G in heart tissues on day 3 post-sham operation or post-MI surgery (n = 6 per group). (I) Quantitative analysis of cardiac function parameters EF% and FS% in the five groups on day 21 post-sham operation or post-MI surgery (n = 8 per group) (J) Representative images and quantitative analyses of Masson's trichrome staining of mouse hearts on day 21 post-sham operation or post-MI surgery (Scale bar = 0.5 mm or 50 μm, n = 6 per group) (K) Representative Western blots and quantitative analyses of α-SMA in heart tissues on day 21 post-sham operation or post-MI surgery (n = 6 per group). (L, M) Relative mRNA levels of Col1a1 and Col3a1 detected by RT-qPCR in heart tissues on day 21 post-sham operation or post-MI surgery (n = 6 per group). For female mice: (N) Representative immunofluorescence images and quantitative analysis of Ly6G expression in female mouse hearts on day 3 post-sham operation or post-MI surgery (Scale bar = 50 μm, n = 6 per group). (O) Quantitative analysis of cardiac function parameters EF% and FS% in the five female mice groups on day 3 post-sham operation or post-MI surgery (n = 8 per group). (P) Relative mRNA levels of Col1a1 and Col3a1 detected by RT-qPCR in female mice heart tissues on day 21 post-sham operation or post-MI surgery (n = 6 per group). Data are presented as mean ± SD. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. L-TCS, low-dose TCS; M-TCS, medium-dose TCS; H-TCS, high-dose TCS. TCS, Triclosan; MI, Myocardial Infarction; EF, Ejection Fraction; FS, Fractional Shortening; CK-MB, Creatine Kinase MB Isoenzyme.

Article Snippet: Real-time qPCR assays were conducted on a LightCycler® 96 System (Roche, Switzerland) using ChamQTM SYBR Color qPCR Master Mix (Q411-02, Vazyme, China).

Techniques: Control, Staining, Expressing, Western Blot, Quantitative RT-PCR, Immunofluorescence

Journal: Redox Biology

Article Title: Triclosan exacerbates post-myocardial infarction injury via Nur77 ubiquitination: Linking NTRK2/PGC-1α-mediated mitochondrial dysfunction to senescence and ferroptosis

doi: 10.1016/j.redox.2026.104022

Figure Lengend Snippet: TCS exposure exacerbated ferroptosis and mitochondrial dysfunction after ischemic myocardial injury both in mouse models and in NRCMs For male mice: (A ) Relative mRNA levels of Mfn1 and Mfn2 detected by RT-qPCR in heart tissues on day 3 post-sham operation or post-MI surgery (n = 6 per group). (B) Representative Western blots and quantitative analyses of DRP1 and MFN2 in heart tissues on day 3 post-sham operation or post-MI surgery (n = 6 per group). (C) Relative mRNA levels of OXPHOS-related genes detected by RT-qPCR in heart tissues on day 3 post-sham operation or post-MI surgery, including mt-ATP6, mt-Ctyb, mt-Nd1 , mt-Co1 , Cox4i1 , Ndufv1 , Ndufs1 , Ndufb8 , Uqcrc2 , and Sdhb (n = 6 per group). (D) Representative Western blots and quantitative analyses of OXPHOS-related proteins (ATP5A, MTCO1, SDHB, NDUFB8) in DMSO- or TCS-exposed NRCMs following hypoxia stimulation (n = 3 per group). (E, F) Representative images and quantitative analyses of DCFH-DA and MitoSox staining in DMSO- or TCS-exposed NRCMs following hypoxia stimulation (Scale bar = 20 μm, n = 3 per group). (G) Representative Western blots and quantitative analyses of ACSL4 and GPX4 in heart tissues on day 3 post-sham operation or post-MI surgery (n = 6 per group). (H) Representative immunohistochemistry images and quantitative analysis of GPX4 expression levels in heart tissues on day 3 post-MI surgery (Scale bar = 50 μm, n = 6 per group). (I) Relative MDA levels in heart tissues on day 3 post-MI surgery (n = 6 per group). (J) Relative SOD activity in heart tissues on day 3 post-MI surgery (n = 6 per group) (K) Representative Western blots and quantitative analyses of ACSL4 and GPX4 in DMSO- or TCS-exposed NRCMs following hypoxia stimulation (n = 3 per group). (L) Representative images and quantitative analyses of FerroOrange staining in DMSO- or TCS-exposed NRCMs following hypoxia stimulation (Scale bar = 20 μm, n = 3 per group). For female mice: (M) Relative mRNA levels of OXPHOS-related genes detected by RT-qPCR in female mcie heart tissues on day 3 post-sham operation or post-MI surgery, including Sdhb, Ndufv1, mt-ND1 (n = 6 per group). (N–O) Representative Western blots and quantitative analyses of OXPHOS-related proteins (MTCO1, SDHB, NDUFB8), ACSL4 and GPX4 in female mcie heart tissues on day 3 post-sham operation or post-MI surgery (n = 6 per group). Data are presented as mean ± SD. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. TCS, Triclosan; MI, Myocardial Infarction; OXPHOS, Oxidative Phosphorylation; DMSO, Dimethyl Sulfoxide; NRCMs, Neonatal Rat Cardiomyocyte; DCFH-DA, 2′,7′-Dichlorodihydrofluorescein diacetate; MitoSox, Red Mitochondrial Superoxide Indicator; MDA, Malondialdehyde; SOD, Superoxide Dismutase.

Article Snippet: Real-time qPCR assays were conducted on a LightCycler® 96 System (Roche, Switzerland) using ChamQTM SYBR Color qPCR Master Mix (Q411-02, Vazyme, China).

Techniques: Quantitative RT-PCR, Western Blot, Staining, Immunohistochemistry, Expressing, Activity Assay, Phospho-proteomics

Journal: Redox Biology

Article Title: Triclosan exacerbates post-myocardial infarction injury via Nur77 ubiquitination: Linking NTRK2/PGC-1α-mediated mitochondrial dysfunction to senescence and ferroptosis

doi: 10.1016/j.redox.2026.104022

Figure Lengend Snippet: TCS exposure exacerbated cardiomyocyte senescence after ischemic myocardial injury both in mouse models and in NRCMs For male mice: (A) Relative mRNA levels of P21 and P53 detected by RT-qPCR in heart tissues on day 3 post-sham operation or post-MI surgery (n = 6 per group). (B) Representative Western blots and quantitative analyses of P16 and P21 in heart tissues on day 3 post-sham operation or post-MI surgery (n = 6 per group). (C) Relative mRNA levels of SASP-related genes detected by RT-qPCR in heart tissues on day 3 post-sham operation or post-MI surgery, including Ccl2, Cxcl1, Cxcl3, Cxcl10, Edn3, Gdf15, Tgfb2, Il-1β, Il-6, and Tnf-α (n = 6 per group). (D, E) Representative immunohistochemistry images and quantitative analysis of γ-H2AX expression levels in heart tissues on day 3 post-sham operation or post-MI surgery (Scale bar = 50 μm, n = 6 per group). (F, G) Representative fluorescence images of P21 and cTnI co-staining in mouse hearts and quantitative analysis of P21 expression in heart tissues on day 3 post-sham operation or post-MI surgery (Scale bar = 50 μm, n = 6 per group). (H) Relative mRNA levels of P16 , P21 and Glb1 detected by RT-qPCR in DMSO- or TCS-exposed NRCMs following hypoxia stimulation (n = 4 per group). (I) Representative Western blots and quantitative analyses of P16 and P21 in DMSO- or TCS-exposed NRCMs following hypoxia stimulation (n = 3 per group). (J) Relative mRNA levels of SASP-related genes detected by RT-qPCR in DMSO- or TCS-exposed NRCMs following hypoxia stimulation, including Edn3, Gdf15, Tgfb2 (n = 4 per group). (K) Representative fluorescence images and quantitative analyses of P16 staining in DMSO- or TCS-exposed NRCMs following hypoxia stimulation (Scale bar = 10 μm, n = 3 per group). For female mice: (L) Relative mRNA levels of SASP-related genes detected by RT-qPCR in female mcie heart tissues on day 3 post-sham operation or post-MI surgery, including Edn3, Gdf15, Tgfb2 (n = 6 per group). (M) Representative Western blots and quantitative analyses of P21 in female mice heart tissues on day 3 post-sham operation or post-MI surgery (n = 6 per group). Data are presented as mean ± SD. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. TCS, Triclosan; RT-qPCR, Quantitative Reverse Transcription Polymerase Chain Reaction; MI, Myocardial Infarction; SASP, Senescence-associated Secretory Phenotype; DMSO, Dimethyl Sulfoxide; NRCMs, Neonatal Rat Cardiomyocyte.

Article Snippet: Real-time qPCR assays were conducted on a LightCycler® 96 System (Roche, Switzerland) using ChamQTM SYBR Color qPCR Master Mix (Q411-02, Vazyme, China).

Techniques: Quantitative RT-PCR, Western Blot, Immunohistochemistry, Expressing, Fluorescence, Staining, Reverse Transcription, Polymerase Chain Reaction

Journal: Redox Biology

Article Title: Triclosan exacerbates post-myocardial infarction injury via Nur77 ubiquitination: Linking NTRK2/PGC-1α-mediated mitochondrial dysfunction to senescence and ferroptosis

doi: 10.1016/j.redox.2026.104022

Figure Lengend Snippet: TCS exposure in human cardiomyocytes exacerbated hypoxia-induced mitochondrial dysfunction-dependent ROS burst and promoted ferroptosis and senescence. (A) Representative fluorescence images and quantitative analysis of JC-1 staining in DMSO- or TCS-exposed AC16 cells following hypoxia stimulation (Scale bar = 20 μm, n = 3 per group). (B) Representative Western blots and quantitative analyses of OXPHOS-related proteins (ATP5A, MTCO1, SDHB, NDUFB8) in DMSO- or TCS-exposed AC16 cells following hypoxia stimulation (n = 3 per group). (C, D) Representative images and quantitative analyses of DCFH-DA and MitoSox staining in DMSO- or TCS-exposed AC16 cells following hypoxia stimulation (Scale bar = 20 μm, n = 3 per group). (E) Relative mRNA levels of P16, P21, P53 and Glb1 detected by RT-qPCR in DMSO- or TCS-exposed AC16 cells following hypoxia stimulation (n = 3 per group). (F) Representative Western blots and quantitative analyses of P16 and P21 in DMSO- or TCS-exposed AC16 cells following hypoxia stimulation (n = 3 per group). (G – I) Representative fluorescence images and quantitative analysis of P16 and P21 staining in DMSO- or TCS-exposed AC16 cells following hypoxia stimulation (Scale bar = 10 μm, n = 3 per group). (J) Relative mRNA levels of SASP-related genes detected by RT-qPCR in DMSO- or TCS-exposed AC16 cells following hypoxia stimulation, including CXCL1, CXCL10, IL-1β, IL-6, MMP1, MMP3, GDF15 , and EDN3. (n = 3 per group). (K, L) Representative Western blots and quantitative analyses of ACSL4 and GPX4 in DMSO- or TCS-exposed AC16 cells following hypoxia stimulation (n = 3 per group). ( M ) Relative MDA levels in AC16 cells across two groups (Scale bar = 10 μm, n = 3 per group). ( N ) Representative images of FerroOrange staining in AC16 cells across two groups (Scale bar = 10 μm, n = 3 per group). Data are presented as mean ± SD. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. TCS, Triclosan; DMSO, Dimethyl Sulfoxide; DCFH-DA, 2′,7′-Dichlorodihydrofluorescein diacetate; OXPHOS, Oxidative Phosphorylation; MitoSox, Red Mitochondrial Superoxide Indicator; RT-qPCR, Quantitative Reverse Transcription Polymerase Chain Reaction; SASP, Senescence-associated Secretory Phenotype; MDA, Malondialdehyde.

Article Snippet: Real-time qPCR assays were conducted on a LightCycler® 96 System (Roche, Switzerland) using ChamQTM SYBR Color qPCR Master Mix (Q411-02, Vazyme, China).

Techniques: Fluorescence, Staining, Western Blot, Quantitative RT-PCR, Phospho-proteomics, Reverse Transcription, Polymerase Chain Reaction

Journal: Redox Biology

Article Title: Triclosan exacerbates post-myocardial infarction injury via Nur77 ubiquitination: Linking NTRK2/PGC-1α-mediated mitochondrial dysfunction to senescence and ferroptosis

doi: 10.1016/j.redox.2026.104022

Figure Lengend Snippet: NTRK2 is identified as a pivotal downstream molecule mediating TCS-induced aggravation of ischemic myocardial injury. (A) Relative mRNA levels of Ntrk2 detected by RT-qPCR in heart tissues on day 3 post-MI surgery (Scale bar = 50 μm, n = 4 per group). (B) Representative immunohistochemistry images and quantitative analysis of NTRK2 expression levels in heart tissues on day 3 post-sham operation or post-MI surgery (n = 3 per group). (C) Representative fluorescence images and quantitative analyses of MitoSox staining in hypoxia-stimulated AC16 cells following exposure to DMSO, ANA-12, TCS, or co-exposure to TCS and ANA-12 (Scale bar = 20 μm, n = 3 per group). (D) Relative mRNA levels of P16 and P21 detected by RT-qPCR in hypoxia-stimulated AC16 cells following exposure to DMSO, ANA-12, TCS, or co-exposure to TCS and ANA-12 (n = 3 per group). (E) Representative Western blots and quantitative analyses of P16 and P21 in hypoxia-stimulated AC16 cells following exposure to DMSO, ANA-12, TCS, or co-exposure to TCS and ANA-12 (n = 3 per group). (F, G) Representative fluorescence images and quantitative analysis of γ-H2AX staining in hypoxia-stimulated AC16 cells across four groups (Scale bar = 10 μm, n = 3 per group). (H) Relative mRNA levels of SASP-related genes detected by RT-qPCR in hypoxia-stimulated AC16 cells across four groups, including Edn3, Gdf15, Tgfb2, and Il-1β (n = 3 per group). (I – J) Representative fluorescence images and quantitative analyses of FerroOrange staining in hypoxia-stimulated AC16 cells across four groups (Scale bar = 10 μm, n = 3 per group). (K) Relative mRNA levels of Acsl4 and Gpx4 detected by RT-qPCR in hypoxia-stimulated AC16 cells across four groups (n = 3 per group). (L) Representative Western blots and quantitative analyses of ACSL4 and GPX4 in hypoxia-stimulated AC16 cells across four groups (n = 3 per group). (M) Representative echocardiographic images and quantitative analyses of EF% and FS% in MI mice after 8 weeks of TCS exposure with/without ANA-12 treatment (n = 4 per group). (N) Representative Western blots and quantitative analyses of ACSL4, GPX4, P16, and P21 in MI mice 3 days post-infarction after 8 weeks of TCS exposure with/without ANA-12 treatment (n = 4 per group). (O) Representative Western blots and quantitative analyses of α-SMA and Col3a1 in MI mice 21 days post-infarction after 8 weeks of TCS exposure with/without ANA-12 treatment (n = 4 per group). Data are presented as mean ± SD. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. TCS, Triclosan; RT-qPCR, Quantitative Reverse Transcription Polymerase Chain Reaction; MI, Myocardial Infarction; MitoSox, Red Mitochondrial Superoxide Indicator; DMSO, Dimethyl Sulfoxide; SASP, Senescence-associated Secretory Phenotype; EF, Ejection Fraction; FS, Fractional Shortening.

Article Snippet: Real-time qPCR assays were conducted on a LightCycler® 96 System (Roche, Switzerland) using ChamQTM SYBR Color qPCR Master Mix (Q411-02, Vazyme, China).

Techniques: Quantitative RT-PCR, Immunohistochemistry, Expressing, Fluorescence, Staining, Western Blot, Reverse Transcription, Polymerase Chain Reaction

Journal: Redox Biology

Article Title: Triclosan exacerbates post-myocardial infarction injury via Nur77 ubiquitination: Linking NTRK2/PGC-1α-mediated mitochondrial dysfunction to senescence and ferroptosis

doi: 10.1016/j.redox.2026.104022

Figure Lengend Snippet: Nur77/NTRK2 axis regulated senescence and ferroptosis after TCS-induced aggravation of ischemic myocardial injury (A, B) Representative echocardiographic images and quantitative analyses of EF% and FS% at 3 days post-MI in mice with 8-week TCS exposure, followed by MI induction, and treatment with AAV9.cTnT.GFP or AAV9.cTnT.NTRK2, with or without Nur77-KO (n = 5 per group). (C) Relative mRNA levels of P16 and P21 in mouse hearts at 3 days post-MI across four groups (n = 5 per group). (D) Representative Western blots and quantitative analyses of P16 and P21 in mouse hearts at 3 days post-MI across four groups (n = 5 per group). (E) Relative mRNA levels of SASP-related genes ( Edn3, Gdf15, Tgfb2 ) by RT-qPCR in mouse hearts at 3 days post-MI (n = 5 per group). (F) Representative immunohistochemistry images and quantitative analysis of GLB1 in mouse hearts at 3 days post-MI across four groups (Scale bar = 50 μm, n = 5 per group). (G) Representative Western blots and quantitative analyses of ACSL4 and GPX4 in mouse hearts at 3 days post-MI across four groups (n = 5 per group). (H) Quantitative analyses of EF% and FS% at 21 days post-MI in mice with 8-week TCS exposure, followed by MI induction, and treatment with AAV9.cTnT.GFP or AAV9.cTnT.NTRK2, with or without Nur77-KO (n = 5 per group). (I) Relative mRNA levels of P16 and P21 in mouse hearts at 21 days post-MI across four groups (n = 5 per group). (J) Relative mRNA levels of Col1a1, Col3a1 and Postn in mouse hearts at 21 days post-MI across four groups (n = 5 per group). (K–N) Representative fluorescence images and quantitative analysis of Col1a1 and α-SMA in mouse hearts at 21 days post-MI across four groups (Scale bar = 50 or 100 μm, n = 5 per group). Data are presented as mean ± SD. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. TCS, Triclosan; EF, Ejection Fraction; FS, Fractional Shortening; MI, Myocardial Infarction; SASP, Senescence-associated Secretory Phenotype; RT-qPCR, Quantitative Reverse Transcription Polymerase Chain Reaction.

Article Snippet: Real-time qPCR assays were conducted on a LightCycler® 96 System (Roche, Switzerland) using ChamQTM SYBR Color qPCR Master Mix (Q411-02, Vazyme, China).

Techniques: Western Blot, Quantitative RT-PCR, Immunohistochemistry, Fluorescence, Reverse Transcription, Polymerase Chain Reaction

Journal: Redox Biology

Article Title: Triclosan exacerbates post-myocardial infarction injury via Nur77 ubiquitination: Linking NTRK2/PGC-1α-mediated mitochondrial dysfunction to senescence and ferroptosis

doi: 10.1016/j.redox.2026.104022

Figure Lengend Snippet: Pharmacological activation of PGC-1α with ZLN005 mitigated TCS-induced exacerbation of post-MI injury. Mice received 8 weeks of TCS exposure. Four weeks before inducing MI, mice were treated with or without ZLN005 during the last 6 weeks of the 8-week TCS exposure. All panels show analyses in hearts of mice at specific time points post-MI. 3 Days Post-MI (A – F):(A) Representative echocardiographic images and quantitative analyses of EF% and FS%. (n = 4 per group). (B) Representative Western blots and quantitative analyses of OXPHOS-related proteins (ATP5A, MTCO1, SDHB). (n = 4 per group). (C) Relative mRNA levels of OXPHOS-related genes ( mt-ATP6 , mt-ND1 , mt-Cytb , mt-Co1, Ndufb8, Uqcrc2, Cox4i1, Ndufv1, Ndufs1 ) by RT-qPCR. (n = 4 per group). (D) Relative mRNA levels of P16 , P21 , and Glb1 by RT-qPCR. (n = 4 per group). (E) Relative mRNA levels of SASP-related genes ( Cxcl1, Cxcl3, Cxcl10, Edn3, Gdf15, Il-6 ) by RT-qPCR. (n = 4 per group). (F) Representative Western blots and quantitative analyses of ACSL4, GPX4, P16, P21. (n = 4 per group). 21 Days Post-MI (G – K): (G) Representative echocardiographic images and quantitative analyses of EF% and FS%. (n = 4 per group). (H) Relative mRNA levels of P16 and P2 1 by RT-qPCR. (n = 4 per group). (I) Relative mRNA levels of Col1a1, Col3a1 , and Postn by RT-qPCR. (n = 4 per group). (J) Representative Western blots and quantitative analyses of α-SMA and Col3a1. (n = 4 per group). (K) Representative images and quantitative analyses of Masson's trichrome staining (Scale bar = 50 μm, n = 4 per group). Data are presented as mean ± SD. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. TCS, Triclosan; MI, Myocardial Infarction; EF, Ejection Fraction; FS, Fractional Shortening; OXPHOS, Oxidative Phosphorylation; SASP, Senescence-associated Secretory Phenotype; RT-qPCR, Quantitative Reverse Transcription Polymerase Chain Reaction.

Article Snippet: Real-time qPCR assays were conducted on a LightCycler® 96 System (Roche, Switzerland) using ChamQTM SYBR Color qPCR Master Mix (Q411-02, Vazyme, China).

Techniques: Activation Assay, Western Blot, Quantitative RT-PCR, Staining, Phospho-proteomics, Reverse Transcription, Polymerase Chain Reaction