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antibody against pin1  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc antibody against pin1
    Antibody Against Pin1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 4971 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibody+against+pin1/HA-Tag+Rabbit+mAb/pm41831815-108-22-25
    Average 99 stars, based on 4971 article reviews
    antibody against pin1 - by Bioz Stars, 2026-10
    99/100 stars

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    Related Articles

    Blocking Assay:

    Article Title: PIN1 suppresses bladder cancer progression by inducing cellular senescence and activating the interferon response pathway.
    Article Snippet: Background: Bladder cancer (BCa) represents the most frequently malignancies of the urinary system with high recurrence rates and heterogeneous outcomes.. While peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1) is recognized as an oncogene in multiple cancers, its expression pattern, biological function, and the molecular basis of bladder tumorigenesis is still poorly understood.. Methods: We performed comprehensive single-cell RNA sequencing (scRNA-seq) analysis to characterize the cellular heterogeneity of BCa tumor microenvironment and identify malignant epithelial cells.

    Incubation:

    Article Title: PIN1 suppresses bladder cancer progression by inducing cellular senescence and activating the interferon response pathway.
    Article Snippet: Background: Bladder cancer (BCa) represents the most frequently malignancies of the urinary system with high recurrence rates and heterogeneous outcomes.. While peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1) is recognized as an oncogene in multiple cancers, its expression pattern, biological function, and the molecular basis of bladder tumorigenesis is still poorly understood.. Methods: We performed comprehensive single-cell RNA sequencing (scRNA-seq) analysis to characterize the cellular heterogeneity of BCa tumor microenvironment and identify malignant epithelial cells.

    Article Title: Self-assembling heterodimeric prodrug nanoparticles for dual-targeted cancer therapy via the disruption of redox homeostasis and Pin1 degradation.
    Article Snippet: Disrupting redox balance by elevating reactive oxygen species (ROS) selectively induces cancer cell death while sparing healthy tissues.. Peptidyl-prolyl isomerase (Pin1) is overexpressed in several cancer cells and plays a critical role in tumorigenesis and tumor progression.. All-trans retinoic acid (RA) is known to induce cell death by generating ROS and directly binding the active site of Pin1, leading to cancer cell death.

    Binding Assay:

    Article Title: Self-assembling heterodimeric prodrug nanoparticles for dual-targeted cancer therapy via the disruption of redox homeostasis and Pin1 degradation.
    Article Snippet: Disrupting redox balance by elevating reactive oxygen species (ROS) selectively induces cancer cell death while sparing healthy tissues.. Peptidyl-prolyl isomerase (Pin1) is overexpressed in several cancer cells and plays a critical role in tumorigenesis and tumor progression.. All-trans retinoic acid (RA) is known to induce cell death by generating ROS and directly binding the active site of Pin1, leading to cancer cell death.

    Control:

    Article Title: Self-assembling heterodimeric prodrug nanoparticles for dual-targeted cancer therapy via the disruption of redox homeostasis and Pin1 degradation.
    Article Snippet: Disrupting redox balance by elevating reactive oxygen species (ROS) selectively induces cancer cell death while sparing healthy tissues.. Peptidyl-prolyl isomerase (Pin1) is overexpressed in several cancer cells and plays a critical role in tumorigenesis and tumor progression.. All-trans retinoic acid (RA) is known to induce cell death by generating ROS and directly binding the active site of Pin1, leading to cancer cell death.

    Membrane:

    Article Title: Self-assembling heterodimeric prodrug nanoparticles for dual-targeted cancer therapy via the disruption of redox homeostasis and Pin1 degradation.
    Article Snippet: Disrupting redox balance by elevating reactive oxygen species (ROS) selectively induces cancer cell death while sparing healthy tissues.. Peptidyl-prolyl isomerase (Pin1) is overexpressed in several cancer cells and plays a critical role in tumorigenesis and tumor progression.. All-trans retinoic acid (RA) is known to induce cell death by generating ROS and directly binding the active site of Pin1, leading to cancer cell death.



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    Proteintech antibodies against pin1
    A. Western blot of SDS insoluble <t>PIN1,</t> 6 young and 6 old. B . Western blot of SDS insoluble CST3, 6 young and 6 old. C . Western blot of Sarkosyl insoluble MAPT (Tau), 4 young and 4 geriatric. D . Western blot of sarkosyl insoluble HTT, 4 young and 4 geriatric. For all blots each lane represents an independent biological sample (individual donor).
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    A. Western blot of SDS insoluble <t>PIN1,</t> 6 young and 6 old. B . Western blot of SDS insoluble CST3, 6 young and 6 old. C . Western blot of Sarkosyl insoluble MAPT (Tau), 4 young and 4 geriatric. D . Western blot of sarkosyl insoluble HTT, 4 young and 4 geriatric. For all blots each lane represents an independent biological sample (individual donor).
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    Cell Signaling Technology Inc antibodies against pin1
    A. Western blot of SDS insoluble <t>PIN1,</t> 6 young and 6 old. B . Western blot of SDS insoluble CST3, 6 young and 6 old. C . Western blot of Sarkosyl insoluble MAPT (Tau), 4 young and 4 geriatric. D . Western blot of sarkosyl insoluble HTT, 4 young and 4 geriatric. For all blots each lane represents an independent biological sample (individual donor).
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    Santa Cruz Biotechnology antibody against pin 1
    A. Western blot of SDS insoluble <t>PIN1,</t> 6 young and 6 old. B . Western blot of SDS insoluble CST3, 6 young and 6 old. C . Western blot of Sarkosyl insoluble MAPT (Tau), 4 young and 4 geriatric. D . Western blot of sarkosyl insoluble HTT, 4 young and 4 geriatric. For all blots each lane represents an independent biological sample (individual donor).
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    Danaher Inc antibodies against pin1
    <t>PIN1</t> is highly expressed in M5-induced HaCaT cells. (A) The mRNA expression and protein levels of PIN1 in M5-induced or untreated HaCaT cells were detected by RT-qPCR and western blot analysis. (B) The mRNA expression and protein levels of PIN1 in HaCaT cells transfected with sh-PIN1 were detected by RT-qPCR and western blot analysis. (C) The mRNA expression and protein levels of PIN1 in M5-induced HaCaT cells after transfection with sh-PIN1 were detected by RT-qPCR and western blot analysis. Results are the mean ± SD. * P<0.05 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; RT-qPCR, reverse transcription-quantitative PCR; SD, standard deviation; shRNA, short hairpin RNA; NC, negative control.
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    Image Search Results


    A. Western blot of SDS insoluble PIN1, 6 young and 6 old. B . Western blot of SDS insoluble CST3, 6 young and 6 old. C . Western blot of Sarkosyl insoluble MAPT (Tau), 4 young and 4 geriatric. D . Western blot of sarkosyl insoluble HTT, 4 young and 4 geriatric. For all blots each lane represents an independent biological sample (individual donor).

    Journal: bioRxiv

    Article Title: Shifts in protein aggregate stability define proteostasis decline in the aging human brain

    doi: 10.64898/2026.03.27.714902

    Figure Lengend Snippet: A. Western blot of SDS insoluble PIN1, 6 young and 6 old. B . Western blot of SDS insoluble CST3, 6 young and 6 old. C . Western blot of Sarkosyl insoluble MAPT (Tau), 4 young and 4 geriatric. D . Western blot of sarkosyl insoluble HTT, 4 young and 4 geriatric. For all blots each lane represents an independent biological sample (individual donor).

    Article Snippet: Membranes were blocked in 5% non-fat milk in TBS-T for 1 hour at room temperature, then incubated overnight at 4°C on a rocker with primary antibodies against PIN1 (mouse monoclonal, 1:2000, Cat. No. 68127-1-Ig, Proteintech), Cystatin C (CST3 rabbit polyclonal, 1:6000, Cat. No. 12245-1-AP, Proteintech), total tau (Tau5, mouse monoclonal, 1:500, Cat. No. AHB0042, Invitrogen), and HTT (rabbit polyclonal, N-terminal, 1:150, Cat. No. H7540, Sigma-Aldrich).

    Techniques: Western Blot

    PIN1 is highly expressed in M5-induced HaCaT cells. (A) The mRNA expression and protein levels of PIN1 in M5-induced or untreated HaCaT cells were detected by RT-qPCR and western blot analysis. (B) The mRNA expression and protein levels of PIN1 in HaCaT cells transfected with sh-PIN1 were detected by RT-qPCR and western blot analysis. (C) The mRNA expression and protein levels of PIN1 in M5-induced HaCaT cells after transfection with sh-PIN1 were detected by RT-qPCR and western blot analysis. Results are the mean ± SD. * P<0.05 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; RT-qPCR, reverse transcription-quantitative PCR; SD, standard deviation; shRNA, short hairpin RNA; NC, negative control.

    Journal: Experimental and Therapeutic Medicine

    Article Title: PIN1‑silencing mitigates keratinocyte proliferation and the inflammatory response in psoriasis by activating mitochondrial autophagy

    doi: 10.3892/etm.2024.12691

    Figure Lengend Snippet: PIN1 is highly expressed in M5-induced HaCaT cells. (A) The mRNA expression and protein levels of PIN1 in M5-induced or untreated HaCaT cells were detected by RT-qPCR and western blot analysis. (B) The mRNA expression and protein levels of PIN1 in HaCaT cells transfected with sh-PIN1 were detected by RT-qPCR and western blot analysis. (C) The mRNA expression and protein levels of PIN1 in M5-induced HaCaT cells after transfection with sh-PIN1 were detected by RT-qPCR and western blot analysis. Results are the mean ± SD. * P<0.05 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; RT-qPCR, reverse transcription-quantitative PCR; SD, standard deviation; shRNA, short hairpin RNA; NC, negative control.

    Article Snippet: Subsequently, the membranes were blocked with 5% skim milk for 1 h at 25˚C, and successively incubated with primary antibodies against PIN1 (1:1,000; cat. no. ab192036; Abcam), keratin (KRT)1 (1:1,000; cat. no. ab185628; Abcam), KRT6B (1:1,000; cat. no. ab154313; Abcam), cyclooxygenase-2 (Cox2; 1:1,000; cat. no. ab179800; Abcam), inducible nitric oxide synthase (iNOS; 1:1,000; cat. no. ab178945; Abcam), LC3B (1:1,000; cat. no. ab63817; Abcam), Beclin-1 (1:1,000; cat. no. ab207612; Abcam), PTEN induced kinase 1 (PINK1; 1:1,000; cat. no. ab216144; Abcam), Parkin (1:1,000; cat. no. ab77924; Abcam), p62 (1:1,000; cat. no. ab207305; Abcam), COX IV (1:1,000; cat. no. ab16056; Abcam) or GAPDH (1:1,000; cat. no. ab8245; Abcam) overnight at 4˚C.

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Transfection, Reverse Transcription, Real-time Polymerase Chain Reaction, Standard Deviation, shRNA, Negative Control

    PIN1 silencing inhibits M5-induced hyperproliferation in HaCaT cells. (A) Cell Counting Kit-8 assay was used to assess cell viability. (B) EdU staining was performed to assess cell proliferation (magnification, x200). (C) The protein levels of KRT1 and KRT6 in HaCaT cells transfected with sh-PIN1 were detected by western blot analysis. Results are the mean ± SD. ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; KRT, keratin; SD, standard deviation; shRNA, short hairpin RNA; NC, negative control.

    Journal: Experimental and Therapeutic Medicine

    Article Title: PIN1‑silencing mitigates keratinocyte proliferation and the inflammatory response in psoriasis by activating mitochondrial autophagy

    doi: 10.3892/etm.2024.12691

    Figure Lengend Snippet: PIN1 silencing inhibits M5-induced hyperproliferation in HaCaT cells. (A) Cell Counting Kit-8 assay was used to assess cell viability. (B) EdU staining was performed to assess cell proliferation (magnification, x200). (C) The protein levels of KRT1 and KRT6 in HaCaT cells transfected with sh-PIN1 were detected by western blot analysis. Results are the mean ± SD. ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; KRT, keratin; SD, standard deviation; shRNA, short hairpin RNA; NC, negative control.

    Article Snippet: Subsequently, the membranes were blocked with 5% skim milk for 1 h at 25˚C, and successively incubated with primary antibodies against PIN1 (1:1,000; cat. no. ab192036; Abcam), keratin (KRT)1 (1:1,000; cat. no. ab185628; Abcam), KRT6B (1:1,000; cat. no. ab154313; Abcam), cyclooxygenase-2 (Cox2; 1:1,000; cat. no. ab179800; Abcam), inducible nitric oxide synthase (iNOS; 1:1,000; cat. no. ab178945; Abcam), LC3B (1:1,000; cat. no. ab63817; Abcam), Beclin-1 (1:1,000; cat. no. ab207612; Abcam), PTEN induced kinase 1 (PINK1; 1:1,000; cat. no. ab216144; Abcam), Parkin (1:1,000; cat. no. ab77924; Abcam), p62 (1:1,000; cat. no. ab207305; Abcam), COX IV (1:1,000; cat. no. ab16056; Abcam) or GAPDH (1:1,000; cat. no. ab8245; Abcam) overnight at 4˚C.

    Techniques: Cell Counting, Staining, Transfection, Western Blot, Standard Deviation, shRNA, Negative Control

    PIN1 silencing inhibits M5-induced inflammation in HaCaT cells. (A) The levels of IL-1β, IL-6, IL-8 and IL-23A were measured by ELISA. (B) The protein levels of Cox2 and iNOS in M5-induced HaCaT cells transfected with sh-PIN1 were detected by western blot analysis. Results are the mean ± SD. ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; Cox2, cyclooxygenase-2; iNOS, inducible nitric oxide synthase; shRNA, short hairpin RNA; SD, standard deviation; NC, negative control.

    Journal: Experimental and Therapeutic Medicine

    Article Title: PIN1‑silencing mitigates keratinocyte proliferation and the inflammatory response in psoriasis by activating mitochondrial autophagy

    doi: 10.3892/etm.2024.12691

    Figure Lengend Snippet: PIN1 silencing inhibits M5-induced inflammation in HaCaT cells. (A) The levels of IL-1β, IL-6, IL-8 and IL-23A were measured by ELISA. (B) The protein levels of Cox2 and iNOS in M5-induced HaCaT cells transfected with sh-PIN1 were detected by western blot analysis. Results are the mean ± SD. ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; Cox2, cyclooxygenase-2; iNOS, inducible nitric oxide synthase; shRNA, short hairpin RNA; SD, standard deviation; NC, negative control.

    Article Snippet: Subsequently, the membranes were blocked with 5% skim milk for 1 h at 25˚C, and successively incubated with primary antibodies against PIN1 (1:1,000; cat. no. ab192036; Abcam), keratin (KRT)1 (1:1,000; cat. no. ab185628; Abcam), KRT6B (1:1,000; cat. no. ab154313; Abcam), cyclooxygenase-2 (Cox2; 1:1,000; cat. no. ab179800; Abcam), inducible nitric oxide synthase (iNOS; 1:1,000; cat. no. ab178945; Abcam), LC3B (1:1,000; cat. no. ab63817; Abcam), Beclin-1 (1:1,000; cat. no. ab207612; Abcam), PTEN induced kinase 1 (PINK1; 1:1,000; cat. no. ab216144; Abcam), Parkin (1:1,000; cat. no. ab77924; Abcam), p62 (1:1,000; cat. no. ab207305; Abcam), COX IV (1:1,000; cat. no. ab16056; Abcam) or GAPDH (1:1,000; cat. no. ab8245; Abcam) overnight at 4˚C.

    Techniques: Enzyme-linked Immunosorbent Assay, Transfection, Western Blot, shRNA, Standard Deviation, Negative Control

    Knockdown of PIN1 activates M5-induced mitochondrial autophagy in HaCaT cells. (A) The levels of LC3 and MitoTraker in double-stained cells were measured by immunofluorescence assay (magnification, x200). (B) The protein levels of LC3II/LC3I, Beclin-1, PINK1, Parkin (mitochondrion), p62 and Parkin (cytoplasm) in M5-induced HaCaT cells transfected with sh-PIN1 were detected by western blot analysis. (C) JC-1 staining was used to assess the mitochondrial membrane potential (magnification, x200). Results are the mean ± SD. * P<0.05, ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; Cox, cyclooxygenase; shRNA, short hairpin RNA; NC, negative control; SD, standard deviation.

    Journal: Experimental and Therapeutic Medicine

    Article Title: PIN1‑silencing mitigates keratinocyte proliferation and the inflammatory response in psoriasis by activating mitochondrial autophagy

    doi: 10.3892/etm.2024.12691

    Figure Lengend Snippet: Knockdown of PIN1 activates M5-induced mitochondrial autophagy in HaCaT cells. (A) The levels of LC3 and MitoTraker in double-stained cells were measured by immunofluorescence assay (magnification, x200). (B) The protein levels of LC3II/LC3I, Beclin-1, PINK1, Parkin (mitochondrion), p62 and Parkin (cytoplasm) in M5-induced HaCaT cells transfected with sh-PIN1 were detected by western blot analysis. (C) JC-1 staining was used to assess the mitochondrial membrane potential (magnification, x200). Results are the mean ± SD. * P<0.05, ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; Cox, cyclooxygenase; shRNA, short hairpin RNA; NC, negative control; SD, standard deviation.

    Article Snippet: Subsequently, the membranes were blocked with 5% skim milk for 1 h at 25˚C, and successively incubated with primary antibodies against PIN1 (1:1,000; cat. no. ab192036; Abcam), keratin (KRT)1 (1:1,000; cat. no. ab185628; Abcam), KRT6B (1:1,000; cat. no. ab154313; Abcam), cyclooxygenase-2 (Cox2; 1:1,000; cat. no. ab179800; Abcam), inducible nitric oxide synthase (iNOS; 1:1,000; cat. no. ab178945; Abcam), LC3B (1:1,000; cat. no. ab63817; Abcam), Beclin-1 (1:1,000; cat. no. ab207612; Abcam), PTEN induced kinase 1 (PINK1; 1:1,000; cat. no. ab216144; Abcam), Parkin (1:1,000; cat. no. ab77924; Abcam), p62 (1:1,000; cat. no. ab207305; Abcam), COX IV (1:1,000; cat. no. ab16056; Abcam) or GAPDH (1:1,000; cat. no. ab8245; Abcam) overnight at 4˚C.

    Techniques: Knockdown, Staining, Immunofluorescence, Transfection, Western Blot, Membrane, shRNA, Negative Control, Standard Deviation

    PIN1 silencing ameliorates M5-induced hyperproliferation in HaCaT cells by activating mitochondrial autophagy. (A) Cell Counting Kit-8 assay was used to assess cell viability. (B) EdU staining was performed to assess cell proliferation (magnification, x200). (C) The protein levels of KRT1 and KRT6 in Mdivi-1-treated HaCaT cells transfected with sh-PIN1 were detected by western blotting. Results are the mean ± SD. ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; KRT, keratin; Mdivi-1, mitochondrial division inhibitor-1; shRNA, short hairpin RNA; SD, standard deviation.

    Journal: Experimental and Therapeutic Medicine

    Article Title: PIN1‑silencing mitigates keratinocyte proliferation and the inflammatory response in psoriasis by activating mitochondrial autophagy

    doi: 10.3892/etm.2024.12691

    Figure Lengend Snippet: PIN1 silencing ameliorates M5-induced hyperproliferation in HaCaT cells by activating mitochondrial autophagy. (A) Cell Counting Kit-8 assay was used to assess cell viability. (B) EdU staining was performed to assess cell proliferation (magnification, x200). (C) The protein levels of KRT1 and KRT6 in Mdivi-1-treated HaCaT cells transfected with sh-PIN1 were detected by western blotting. Results are the mean ± SD. ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; KRT, keratin; Mdivi-1, mitochondrial division inhibitor-1; shRNA, short hairpin RNA; SD, standard deviation.

    Article Snippet: Subsequently, the membranes were blocked with 5% skim milk for 1 h at 25˚C, and successively incubated with primary antibodies against PIN1 (1:1,000; cat. no. ab192036; Abcam), keratin (KRT)1 (1:1,000; cat. no. ab185628; Abcam), KRT6B (1:1,000; cat. no. ab154313; Abcam), cyclooxygenase-2 (Cox2; 1:1,000; cat. no. ab179800; Abcam), inducible nitric oxide synthase (iNOS; 1:1,000; cat. no. ab178945; Abcam), LC3B (1:1,000; cat. no. ab63817; Abcam), Beclin-1 (1:1,000; cat. no. ab207612; Abcam), PTEN induced kinase 1 (PINK1; 1:1,000; cat. no. ab216144; Abcam), Parkin (1:1,000; cat. no. ab77924; Abcam), p62 (1:1,000; cat. no. ab207305; Abcam), COX IV (1:1,000; cat. no. ab16056; Abcam) or GAPDH (1:1,000; cat. no. ab8245; Abcam) overnight at 4˚C.

    Techniques: Cell Counting, Staining, Transfection, Western Blot, shRNA, Standard Deviation

    PIN1 silencing ameliorates M5-induced inflammation of HaCaT cells by activating mitochondrial autophagy. (A) The levels of IL-1β, IL-6, IL-8 and IL-23A were measured by ELISA. (B) The protein levels of Cox2 and iNOS in Mdivi-1-treated HaCaT cells transfected with sh-PIN1 were detected by western blot analysis. Results are the mean ± SD. ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; Cox2, cyclooxygenase-2; iNOS, inducible nitric oxide synthase; Mdivi-1, mitochondrial division inhibitor-1; shRNA, short hairpin RNA; SD, standard deviation.

    Journal: Experimental and Therapeutic Medicine

    Article Title: PIN1‑silencing mitigates keratinocyte proliferation and the inflammatory response in psoriasis by activating mitochondrial autophagy

    doi: 10.3892/etm.2024.12691

    Figure Lengend Snippet: PIN1 silencing ameliorates M5-induced inflammation of HaCaT cells by activating mitochondrial autophagy. (A) The levels of IL-1β, IL-6, IL-8 and IL-23A were measured by ELISA. (B) The protein levels of Cox2 and iNOS in Mdivi-1-treated HaCaT cells transfected with sh-PIN1 were detected by western blot analysis. Results are the mean ± SD. ** P<0.01 and *** P<0.001. PIN1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; Cox2, cyclooxygenase-2; iNOS, inducible nitric oxide synthase; Mdivi-1, mitochondrial division inhibitor-1; shRNA, short hairpin RNA; SD, standard deviation.

    Article Snippet: Subsequently, the membranes were blocked with 5% skim milk for 1 h at 25˚C, and successively incubated with primary antibodies against PIN1 (1:1,000; cat. no. ab192036; Abcam), keratin (KRT)1 (1:1,000; cat. no. ab185628; Abcam), KRT6B (1:1,000; cat. no. ab154313; Abcam), cyclooxygenase-2 (Cox2; 1:1,000; cat. no. ab179800; Abcam), inducible nitric oxide synthase (iNOS; 1:1,000; cat. no. ab178945; Abcam), LC3B (1:1,000; cat. no. ab63817; Abcam), Beclin-1 (1:1,000; cat. no. ab207612; Abcam), PTEN induced kinase 1 (PINK1; 1:1,000; cat. no. ab216144; Abcam), Parkin (1:1,000; cat. no. ab77924; Abcam), p62 (1:1,000; cat. no. ab207305; Abcam), COX IV (1:1,000; cat. no. ab16056; Abcam) or GAPDH (1:1,000; cat. no. ab8245; Abcam) overnight at 4˚C.

    Techniques: Enzyme-linked Immunosorbent Assay, Transfection, Western Blot, shRNA, Standard Deviation