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anti p mlkl  (Boster Bio)


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    Structured Review

    Boster Bio anti p mlkl
    Anti P Mlkl, supplied by Boster Bio, used in various techniques. Bioz Stars score: 92/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+p+mlkl/Anti-Phospho-MLKL+(S345)+Rabbit+Monoclonal+Antibody/pm41862445-182-144-145
    Average 92 stars, based on 5 article reviews
    anti p mlkl - by Bioz Stars, 2026-09
    92/100 stars

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    other:

    Article Title: FAK/SRC-JNK axis promotes ferroptosis via upregulating ACSL4 expression
    Article Snippet: Primary antibodies used were anti-FAK (proteintech, Cat#66258-1-Ig), anti-SRC (proteintech, Cat#60315-1-Ig), anti-JNK1 (proteintech, Cat#66210-1-Ig), anti-JNK2 (PTMALO, Cat#PTM-6948), anti-ACSL4 (SANTA CRUZ, Cat#sc365230), anti-SMAD4 (proteintech, Cat#10231-1-AP), anti-SMAD4 (MCE, Cat#HY- P80326 ), anti-Phospho-FAK-Ser708 (Wanleibio, Cat#WL02764), anti-Phospho-SRC-Tyr530 (Wanleibio, Cat#WL02114), anti-Phospho-JNK-Thr183/Tyr185 (Wanleibio, Cat#WL01813), anti-GAPDH (proteintech, Cat#60004-1-Ig). anti-NFATC1 (Wanleibio, Cat#WL01632), anti-NFATC1 (SANTA CRUZ, Cat#sc-7294), anti-NFATC3 (SANTA CRUZ, Cat#sc-8405), anti-ATF2 (SANTA CRUZ, Cat#sc-242), anti-ELK1 (proteintech, Cat#27420-1-AP), anti-ELK1 (PTM BIO, Cat#20042), anti-STAT3 (SANTA CRUZ, Cat#sc-8019), anti-p-ELK1 (SANTA CRUZ, Cat#sc-8406), anti-p-NFATC3 (SANTA CRUZ, Cat#sc-365785), anti-c-Jun (CST, Cat#9165), anti-c-Jun (proteintech, Cat#24909-1-AP), anti-p-c-Jun (SANTA CRUZ, Cat#sc-8322), anti-p-ATF2 (SANTA CRUZ, Cat#sc-8398), anti-HSF1 (SANTA CRUZ, Cat#sc-17757), anti-SLC7A11 (proteintech, Cat#26864-1-AP), anti-GPX4 (abcam, Cat#ab231174), anti-alpha Tubulin (proteintech, Cat#11224-1-AP), anti-ATP1A1 (proteintech, Cat#14418-1-AP), anti-Histone H3 (Wanleibio, Cat#WL0984a), anti-MBOAT1 (proteintech, Cat#25615-1-AP), anti-MBOAT2 (abcepta, Cat#AP17786c), anti-DHODH (proteintech, Cat#14877-1-AP), anti-ALOX15 (abcam Cat#244205), anti-4-Hydroxynonenal (Thermo fisher, Cat# MA5-27570), anti-NCOA4 (proteintech, Cat#10727-1-AP), anti-FTH1 (HUABIO, Cat#ET1705-55) and anti-FTL1 (Affinity, Cat#DF6604), anti-RIP3 (HUABIO cat#HA722183), anti-p-RIP3 (HUABIO cat#HA721428), anti-caspase3 (proteintech, Cat#19677-1-AP), anti-p-MLKL (BOSTER cat# P00535 ), anti-MLKL (proteintech, Cat#66675-1-Ig) Chemical reagents used were erastin (Selleck, Cat#S7242), Defactinib (TargetMOL, Cat#1073154-85-4), Saracatinib (Selleck, Cat#AZDO530), Imidazole ketone erastin (Selleck, Cat#S8877), Kartogenin (Adoop Bioscience, Cat#A12926), DTHIB (TargetMOL, Cat#897326-30-6), HSF1A (TargetMOL, Cat#1196723-93-9), STAT3-IN-1 (TargetMOL, Cat#2059952-75-7), NDMC101 (TargetMOL, Cat#1308631-40-4), BODIPY C11 (Thermo Fisher, Cat# D3861).

    Article Title: FAK/SRC-JNK axis promotes ferroptosis via upregulating ACSL4 expression.
    Article Snippet: Primary antibodies used were anti-FAK (proteintech, Cat#66258-1-Ig), anti-SRC (proteintech, Cat#603151-Ig), anti-JNK1 (proteintech, Cat#66210-1-Ig), anti-JNK2 (PTMALO, Cat#PTM-6948), anti-ACSL4 (SANTA CRUZ, Cat#sc365230), anti-SMAD4 (proteintech, Cat#10231-1-AP), anti-SMAD4 (MCE, Cat#HY-P80326), anti-Phospho-FAK-Ser708 (Wanleibio, Cat#WL02764), anti-Phospho-SRC-Tyr530 (Wanleibio, Cat#WL02114), anti-Phospho-JNK-Thr183/Tyr185 (Wanleibio, Cat#WL01813), antiGAPDH (proteintech, Cat#60004-1-Ig). anti-NFATC1 (Wanleibio, Cat#WL01632), anti-NFATC1 (SANTA CRUZ, Cat#sc-7294), anti-NFATC3 (SANTA CRUZ, Cat#sc-8405), anti-ATF2 (SANTA CRUZ, Cat#sc-242), anti-ELK1 (proteintech, Cat#27420-1-AP), anti-ELK1 (PTM BIO, Cat#20042), anti-STAT3 (SANTA CRUZ, Cat#sc-8019), anti-p-ELK1 (SANTA CRUZ, Cat#sc-8406), anti-p-NFATC3 (SANTA CRUZ, Cat#sc-365785), anti-c-Jun (CST, Cat#9165), anti-c-Jun (proteintech, Cat#24909-1-AP), anti-pc-Jun (SANTA CRUZ, Cat#sc-8322), anti-p-ATF2 (SANTA CRUZ, Cat#sc-8398), anti-HSF1 (SANTA CRUZ, Cat#sc-17757), anti-SLC7A11 (proteintech, Cat#26864-1-AP), anti-GPX4 (abcam, Cat#ab231174), anti-alpha Tubulin (proteintech, Cat#11224-1-AP), anti-ATP1A1 (proteintech, Cat#14418-1-AP), antiHistone H3 (Wanleibio, Cat#WL0984a), anti-MBOAT1 (proteintech, Cat#25615-1-AP), anti-MBOAT2 (abcepta, Cat#AP17786c), anti-DHODH (proteintech, Cat#14877-1-AP), anti-ALOX15 (abcam Cat#244205), anti-4-Hydroxynonenal (Thermo fisher, Cat# MA5-27570), anti-NCOA4 (proteintech, Cat#10727-1-AP), anti-FTH1 (HUABIO, Cat#ET1705-55) and anti-FTL1 (Affinity, Cat#DF6604), anti-RIP3 (HUABIO cat# HA722183), anti-p-RIP3 (HUABIO cat#HA721428), anticaspase3 (proteintech, Cat#19677-1-AP), anti-p-MLKL (BOSTER cat#P00535), anti-MLKL (proteintech, Cat#66675-1-Ig) Chemical reagents used were erastin (Selleck, Cat#S7242), Defactinib (TargetMOL, Cat#1073154-85-4), Saracatinib (Selleck, Cat#AZDO530), Imidazole ketone erastin (Selleck, Cat#S8877), Kartogenin (Adoop Bioscience, Cat#A12926), DTHIB (TargetMOL, Cat#897326-30-6), HSF1A (TargetMOL, Cat#119672393-9), STAT3-IN-1 (TargetMOL, Cat#2059952-75-7), NDMC101 (TargetMOL, Cat#1308631-40-4), AR TI CL E IN P RE SS BODIPY C11 (Thermo Fisher, Cat# D3861).

    Incubation:

    Article Title: IER3 Promotes Non-Small Cell Lung Cancer Malignancy by Suppressing Ferroptosis via the AKT/GSK3β/NRF2 Pathway.
    Article Snippet: Non-small cell lung cancer (NSCLC) remains a lethal malignancy due to therapy resistance and recurrence.. Ferroptosis, a regulated form of cell death, is a promising strategy to overcome cancer drug resistance, yet its mechanisms remain incompletely defined.. Here, we report that Immediate Early Response 3 (IER3) is significantly upregulated in NSCLC tumors and linked to advanced stage and poor prognosis.



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    Effects of Cl‐amidine and DNase I on necroptosis‐related protein expression after TBI. (A) Western blot analysis <t>of</t> <t>RIP1,</t> RIP3, MLKL, P‐RIP1, P‐RIP3, <t>and</t> <t>P‐MLKL</t> protein levels in the cortex of mice from Sham, TBI+Vehicle, TBI+Cl‐amidine, and TBI+DNase I groups. GAPDH was used as the loading control ( n = 4 per group). (B–G) Quantification of relative protein levels of RIP1, RIP3, MLKL, P‐RIP1, P‐RIP3, and P‐MLKL, normalized to GAPDH. Data are shown as mean ± SD ( n = 4 per group). Statistical significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, compared with the indicated groups; ns: not significant.
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    Experimental validation of CHP2 as a predictive biomarker for drug sensitivity and a driver of PANoptosis. ( A – C ) IC 50 growth inhibition curves of HCT116 and SW480 cells treated with first-line chemotherapeutic agents: ( A ) 5-fluorouracil (5-FU), ( B ) Oxaliplatin, and ( C ) Irinotecan. ( D , E ) IC50 curves for targeted agents: ( D ) Ribociclib and ( E ) Lapatinib. ( F ) Western blot analysis of key PANoptosis markers, including <t>p-MLKL</t> (necroptosis), N-GSDMD (pyroptosis), and Cleaved-Caspase 3 (apoptosis), in Control, CHP2-OV, and CHP2-OV-siRNA-3 groups. ( G – J ) Quantitative analysis of protein expression levels normalized to β-actin. Data are presented as mean ±SD from three independent experiments. * p < 0.05, ** p < 0.01.
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    Image Search Results


    Effects of Cl‐amidine and DNase I on necroptosis‐related protein expression after TBI. (A) Western blot analysis of RIP1, RIP3, MLKL, P‐RIP1, P‐RIP3, and P‐MLKL protein levels in the cortex of mice from Sham, TBI+Vehicle, TBI+Cl‐amidine, and TBI+DNase I groups. GAPDH was used as the loading control ( n = 4 per group). (B–G) Quantification of relative protein levels of RIP1, RIP3, MLKL, P‐RIP1, P‐RIP3, and P‐MLKL, normalized to GAPDH. Data are shown as mean ± SD ( n = 4 per group). Statistical significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, compared with the indicated groups; ns: not significant.

    Journal: Brain and Behavior

    Article Title: Study on the Function and Mechanism of Neutrophil Extracellular Traps in Regulating Necroptosis Following Traumatic Brain Injury

    doi: 10.1002/brb3.71275

    Figure Lengend Snippet: Effects of Cl‐amidine and DNase I on necroptosis‐related protein expression after TBI. (A) Western blot analysis of RIP1, RIP3, MLKL, P‐RIP1, P‐RIP3, and P‐MLKL protein levels in the cortex of mice from Sham, TBI+Vehicle, TBI+Cl‐amidine, and TBI+DNase I groups. GAPDH was used as the loading control ( n = 4 per group). (B–G) Quantification of relative protein levels of RIP1, RIP3, MLKL, P‐RIP1, P‐RIP3, and P‐MLKL, normalized to GAPDH. Data are shown as mean ± SD ( n = 4 per group). Statistical significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, compared with the indicated groups; ns: not significant.

    Article Snippet: The membranes were blocked with 5% skimmed milk prepared in TBST (Tris‐buffered saline with 0.1% Tween‐20) at room temperature for 1 h. They were then incubated overnight at 4°C with the following primary antibodies: PAD4 (1:1000, 214810, Abcam), MPO (1:1000, ab208670, Abcam), Bcl‐2 (1:1000, A0208, Abclonal), Bax (1:1000, A19684, Abclonal), RIP1 (1:1000, #3493, Cell Signaling Technology), RIP3 (1:1000, #95702, Cell Signaling Technology), MLKL (1:1000, #37705, Cell Signaling Technology), P‐RIP1 (1:1000, #31122, Cell Signaling Technology), P‐RIP3 (1:1000, #91702, Cell Signaling Technology), P‐MLKL (1:1000, #37333, Cell Signaling Technology), and GAPDH (1:1000, AB‐P‐R001, GOODHERE Biotech).

    Techniques: Expressing, Western Blot, Control

    Experimental validation of CHP2 as a predictive biomarker for drug sensitivity and a driver of PANoptosis. ( A – C ) IC 50 growth inhibition curves of HCT116 and SW480 cells treated with first-line chemotherapeutic agents: ( A ) 5-fluorouracil (5-FU), ( B ) Oxaliplatin, and ( C ) Irinotecan. ( D , E ) IC50 curves for targeted agents: ( D ) Ribociclib and ( E ) Lapatinib. ( F ) Western blot analysis of key PANoptosis markers, including p-MLKL (necroptosis), N-GSDMD (pyroptosis), and Cleaved-Caspase 3 (apoptosis), in Control, CHP2-OV, and CHP2-OV-siRNA-3 groups. ( G – J ) Quantitative analysis of protein expression levels normalized to β-actin. Data are presented as mean ±SD from three independent experiments. * p < 0.05, ** p < 0.01.

    Journal: Cells

    Article Title: Machine Learning-Driven Multi-Omics Analysis Identifies CHP2 as a Key PANoptosis-Related Dual-Function Biomarker in Colorectal Cancer

    doi: 10.3390/cells15050430

    Figure Lengend Snippet: Experimental validation of CHP2 as a predictive biomarker for drug sensitivity and a driver of PANoptosis. ( A – C ) IC 50 growth inhibition curves of HCT116 and SW480 cells treated with first-line chemotherapeutic agents: ( A ) 5-fluorouracil (5-FU), ( B ) Oxaliplatin, and ( C ) Irinotecan. ( D , E ) IC50 curves for targeted agents: ( D ) Ribociclib and ( E ) Lapatinib. ( F ) Western blot analysis of key PANoptosis markers, including p-MLKL (necroptosis), N-GSDMD (pyroptosis), and Cleaved-Caspase 3 (apoptosis), in Control, CHP2-OV, and CHP2-OV-siRNA-3 groups. ( G – J ) Quantitative analysis of protein expression levels normalized to β-actin. Data are presented as mean ±SD from three independent experiments. * p < 0.05, ** p < 0.01.

    Article Snippet: After the protein concentration was determined with a BCA protein assay kit (Beyotime, P0010), identical amounts of proteins were subjected to SDS-PAGE and transferred onto PVDF membranes, which were subsequently incubated with primary antibodies against CHP2 (Boster, Wuhan, China, A08478-2, 1:1000), p-MLKL (MCE, HY86069, 1:1000), GSDMD (N-terminal) (MCE, HY- P85810 , 1:1000), Cleaved Caspase-3 (HY- P86370 ) and β-actin (Servicebio, ZB15001-HRP, 1:2000).

    Techniques: Biomarker Discovery, Inhibition, Western Blot, Control, Expressing