perk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc perk
    Perk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc perk
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    Cell Signaling Technology Inc perk antibody
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    Cell Signaling Technology Inc er kinase
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    Cell Signaling Technology Inc anti perk
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    p erk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p erk
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    anti perk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti perk
    PA provokes hypothalamic leptin resistance and ER stress. Notes: ( A ) mHypoE cells were treated with PA at indicated doses for 24 hours prior to leptin treatment. After 45 minutes, cells were prepared for Western blot analysis. Representative Western blots show levels of phospho-JAK2 <t>(pJAK2),</t> <t>phospho-STAT3</t> (pSTAT3), total-STAT3, and β-Actin levels. ( B , C ) Quantification of pJAK2 and pSTAT3 normalized to β-Actin and total-STAT3, respectively. ( D ) mHypoE cells were treated with PA at indicated doses for 24 hours and subjected to Western blot analysis. The results show the levels of <t>phosphor-PERK</t> (pPERK), total PERK, CHOP, and β-Actin. ( E , F ) Quantification of pPERK and CHOP normalized to total-PERK and β-Actin, respectively. Results were expressed as mean ± SEM of three independent experiments at least. ** P <0.01, *** P <0.001 compared with control groups. Abbreviations: ER, endoplasmic reticulum; JAK2, Janus-activated kinase 2; STAT3, signal transducer and activator of transcription 3.
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    1) Product Images from "Salubrinal abrogates palmitate-induced leptin resistance and endoplasmic reticulum stress via nuclear factor kappa-light-chain-enhancer of activated B cell pathway in mHypoE-44 hypothalamic neurons"

    Article Title: Salubrinal abrogates palmitate-induced leptin resistance and endoplasmic reticulum stress via nuclear factor kappa-light-chain-enhancer of activated B cell pathway in mHypoE-44 hypothalamic neurons

    Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

    doi: 10.2147/DMSO.S179346

    PA provokes hypothalamic leptin resistance and ER stress. Notes: ( A ) mHypoE cells were treated with PA at indicated doses for 24 hours prior to leptin treatment. After 45 minutes, cells were prepared for Western blot analysis. Representative Western blots show levels of phospho-JAK2 (pJAK2), phospho-STAT3 (pSTAT3), total-STAT3, and β-Actin levels. ( B , C ) Quantification of pJAK2 and pSTAT3 normalized to β-Actin and total-STAT3, respectively. ( D ) mHypoE cells were treated with PA at indicated doses for 24 hours and subjected to Western blot analysis. The results show the levels of phosphor-PERK (pPERK), total PERK, CHOP, and β-Actin. ( E , F ) Quantification of pPERK and CHOP normalized to total-PERK and β-Actin, respectively. Results were expressed as mean ± SEM of three independent experiments at least. ** P <0.01, *** P <0.001 compared with control groups. Abbreviations: ER, endoplasmic reticulum; JAK2, Janus-activated kinase 2; STAT3, signal transducer and activator of transcription 3.
    Figure Legend Snippet: PA provokes hypothalamic leptin resistance and ER stress. Notes: ( A ) mHypoE cells were treated with PA at indicated doses for 24 hours prior to leptin treatment. After 45 minutes, cells were prepared for Western blot analysis. Representative Western blots show levels of phospho-JAK2 (pJAK2), phospho-STAT3 (pSTAT3), total-STAT3, and β-Actin levels. ( B , C ) Quantification of pJAK2 and pSTAT3 normalized to β-Actin and total-STAT3, respectively. ( D ) mHypoE cells were treated with PA at indicated doses for 24 hours and subjected to Western blot analysis. The results show the levels of phosphor-PERK (pPERK), total PERK, CHOP, and β-Actin. ( E , F ) Quantification of pPERK and CHOP normalized to total-PERK and β-Actin, respectively. Results were expressed as mean ± SEM of three independent experiments at least. ** P <0.01, *** P <0.001 compared with control groups. Abbreviations: ER, endoplasmic reticulum; JAK2, Janus-activated kinase 2; STAT3, signal transducer and activator of transcription 3.

    Techniques Used: Western Blot

    perk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc perk
    Expression <t>of</t> <t>BiP,</t> <t>PERK,</t> p-eIF2 α , ATF4, and IRE1 α after EGCG treatment. GAPDH was used as the loading control. The densitometry results are from three independent experiments and are expressed as mean ± SEM ( n =3) normalized to GAPDH, ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, relative to their respective controls at each incubation time.
    Perk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2 α /ATF4 and IRE1 α"

    Article Title: Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2 α /ATF4 and IRE1 α

    Journal: BioMed Research International

    doi: 10.1155/2019/3480569

    Expression of BiP, PERK, p-eIF2 α , ATF4, and IRE1 α after EGCG treatment. GAPDH was used as the loading control. The densitometry results are from three independent experiments and are expressed as mean ± SEM ( n =3) normalized to GAPDH, ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, relative to their respective controls at each incubation time.
    Figure Legend Snippet: Expression of BiP, PERK, p-eIF2 α , ATF4, and IRE1 α after EGCG treatment. GAPDH was used as the loading control. The densitometry results are from three independent experiments and are expressed as mean ± SEM ( n =3) normalized to GAPDH, ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, relative to their respective controls at each incubation time.

    Techniques Used: Expressing, Incubation

    Mechanism of action of EGCG in colorectal cancer (CRC). ER stress is induced by EGCG and activates UPR proteins, PERK (with its downstream targets eIF2 α and ATF4), and IRE1 α . Caspase 3/7 activity is also enhanced, indicating apoptosis occurrence in the colorectal cancer cells.
    Figure Legend Snippet: Mechanism of action of EGCG in colorectal cancer (CRC). ER stress is induced by EGCG and activates UPR proteins, PERK (with its downstream targets eIF2 α and ATF4), and IRE1 α . Caspase 3/7 activity is also enhanced, indicating apoptosis occurrence in the colorectal cancer cells.

    Techniques Used: Activity Assay

    endoplasmic reticulum kinase  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc endoplasmic reticulum kinase
    Curcumin treatment significantly inhibits the PERK-eIF2 α -ATF4-CHOP signaling pathway and the cleavage of caspase-12. After curcumin treatment (10 μ M) for 48 h, (a) the mRNA levels of GRP78 and CHOP were detected by qRT-PCR, and (b) Western blot was performed to determine the protein levels of GRP78, PERK, p-eIF2 α , eIF2 α , ATF4, CHOP, and cleaved caspase-12. (c) Protein bands of GRP78, PERK, ATF4, CHOP, and cleaved caspase-12 were quantified by densitometry, and relative protein levels were normalized to GAPDH. (d) Protein bands of p-eIF2 α were quantified by densitometry, and relative protein expression of p-eIF2 α was normalized to eIF2 α . Data are shown as the mean ± SD. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001. GRP78: glucose-regulated protein 78; CHOP: C/EBP homologous protein; PERK: protein <t>kinase-like</t> <t>endoplasmic</t> <t>reticulum</t> kinase; eIF2 α : eukaryotic translation initiation factor 2 α ; ATF4: activating transcription factor 4; qRT-PCR: quantitative real-time polymerase chain reaction.
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    1) Product Images from "Curcumin Improves Epithelial Barrier Integrity of Caco-2 Monolayers by Inhibiting Endoplasmic Reticulum Stress and Subsequent Apoptosis"

    Article Title: Curcumin Improves Epithelial Barrier Integrity of Caco-2 Monolayers by Inhibiting Endoplasmic Reticulum Stress and Subsequent Apoptosis

    Journal: Gastroenterology Research and Practice

    doi: 10.1155/2021/5570796

    Curcumin treatment significantly inhibits the PERK-eIF2 α -ATF4-CHOP signaling pathway and the cleavage of caspase-12. After curcumin treatment (10 μ M) for 48 h, (a) the mRNA levels of GRP78 and CHOP were detected by qRT-PCR, and (b) Western blot was performed to determine the protein levels of GRP78, PERK, p-eIF2 α , eIF2 α , ATF4, CHOP, and cleaved caspase-12. (c) Protein bands of GRP78, PERK, ATF4, CHOP, and cleaved caspase-12 were quantified by densitometry, and relative protein levels were normalized to GAPDH. (d) Protein bands of p-eIF2 α were quantified by densitometry, and relative protein expression of p-eIF2 α was normalized to eIF2 α . Data are shown as the mean ± SD. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001. GRP78: glucose-regulated protein 78; CHOP: C/EBP homologous protein; PERK: protein kinase-like endoplasmic reticulum kinase; eIF2 α : eukaryotic translation initiation factor 2 α ; ATF4: activating transcription factor 4; qRT-PCR: quantitative real-time polymerase chain reaction.
    Figure Legend Snippet: Curcumin treatment significantly inhibits the PERK-eIF2 α -ATF4-CHOP signaling pathway and the cleavage of caspase-12. After curcumin treatment (10 μ M) for 48 h, (a) the mRNA levels of GRP78 and CHOP were detected by qRT-PCR, and (b) Western blot was performed to determine the protein levels of GRP78, PERK, p-eIF2 α , eIF2 α , ATF4, CHOP, and cleaved caspase-12. (c) Protein bands of GRP78, PERK, ATF4, CHOP, and cleaved caspase-12 were quantified by densitometry, and relative protein levels were normalized to GAPDH. (d) Protein bands of p-eIF2 α were quantified by densitometry, and relative protein expression of p-eIF2 α was normalized to eIF2 α . Data are shown as the mean ± SD. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001. GRP78: glucose-regulated protein 78; CHOP: C/EBP homologous protein; PERK: protein kinase-like endoplasmic reticulum kinase; eIF2 α : eukaryotic translation initiation factor 2 α ; ATF4: activating transcription factor 4; qRT-PCR: quantitative real-time polymerase chain reaction.

    Techniques Used: Quantitative RT-PCR, Western Blot, Expressing, Real-time Polymerase Chain Reaction

    endoplasmic reticulum kinase  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc endoplasmic reticulum kinase
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    Cell Signaling Technology Inc anti perk
    HC030031 decreased endoplasmic reticulum oxidative stress through the <t>PERK/eIF2</t> <t>α</t> <t>/ATF-4/CHOP</t> pathway. (a) The related gene expressions of PDLCs in the control group (PDLCs only, C), LPS group (PDLCs treated by LPS, L), LH group (PDLCs treated by 10 μ M HC030031 and LPS, LH), LP group (PDLCs treated by 10 μ M 4-PBA and LPS, LP), LG group (PDLCs treated by 10 μ M GSK2656157 and LPS, LG), and LE group (PDLCs treated by 10 μ M EGTA and LPS, LE) ( n = 4). (b, c) Western blot and semiquantitative statistical analysis of PDLCs in C, L, LH, LP, LG, and LE groups ( n = 3). (d) Total SOD and MDAs of PDLCs in C, L, LH, LP, LG, and LE groups ( n = 4). (e, f) Flow cytometry and quantitative analysis of PDLCs in C, L, LH, LP, LG, and LE groups ( n = 4). Data analysis was performed by using one-way ANOVA and LSD ( ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001). Error bars represent mean ± SEM.
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    1) Product Images from "Inhibition of TRPA1 Ameliorates Periodontitis by Reducing Periodontal Ligament Cell Oxidative Stress and Apoptosis via PERK/eIF2 α /ATF-4/CHOP Signal Pathway"

    Article Title: Inhibition of TRPA1 Ameliorates Periodontitis by Reducing Periodontal Ligament Cell Oxidative Stress and Apoptosis via PERK/eIF2 α /ATF-4/CHOP Signal Pathway

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2022/4107915

    HC030031 decreased endoplasmic reticulum oxidative stress through the PERK/eIF2 α /ATF-4/CHOP pathway. (a) The related gene expressions of PDLCs in the control group (PDLCs only, C), LPS group (PDLCs treated by LPS, L), LH group (PDLCs treated by 10 μ M HC030031 and LPS, LH), LP group (PDLCs treated by 10 μ M 4-PBA and LPS, LP), LG group (PDLCs treated by 10 μ M GSK2656157 and LPS, LG), and LE group (PDLCs treated by 10 μ M EGTA and LPS, LE) ( n = 4). (b, c) Western blot and semiquantitative statistical analysis of PDLCs in C, L, LH, LP, LG, and LE groups ( n = 3). (d) Total SOD and MDAs of PDLCs in C, L, LH, LP, LG, and LE groups ( n = 4). (e, f) Flow cytometry and quantitative analysis of PDLCs in C, L, LH, LP, LG, and LE groups ( n = 4). Data analysis was performed by using one-way ANOVA and LSD ( ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001). Error bars represent mean ± SEM.
    Figure Legend Snippet: HC030031 decreased endoplasmic reticulum oxidative stress through the PERK/eIF2 α /ATF-4/CHOP pathway. (a) The related gene expressions of PDLCs in the control group (PDLCs only, C), LPS group (PDLCs treated by LPS, L), LH group (PDLCs treated by 10 μ M HC030031 and LPS, LH), LP group (PDLCs treated by 10 μ M 4-PBA and LPS, LP), LG group (PDLCs treated by 10 μ M GSK2656157 and LPS, LG), and LE group (PDLCs treated by 10 μ M EGTA and LPS, LE) ( n = 4). (b, c) Western blot and semiquantitative statistical analysis of PDLCs in C, L, LH, LP, LG, and LE groups ( n = 3). (d) Total SOD and MDAs of PDLCs in C, L, LH, LP, LG, and LE groups ( n = 4). (e, f) Flow cytometry and quantitative analysis of PDLCs in C, L, LH, LP, LG, and LE groups ( n = 4). Data analysis was performed by using one-way ANOVA and LSD ( ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001). Error bars represent mean ± SEM.

    Techniques Used: Western Blot, Flow Cytometry

    Schematic diagram of the mechanisms of TRPA1 in periodontitis. TRPA1 inhibition ameliorates periodontitis by reducing oxidative stress and apoptosis via PERK/eIF2 α /ATF-4/CHOP signal pathway in inflammation.
    Figure Legend Snippet: Schematic diagram of the mechanisms of TRPA1 in periodontitis. TRPA1 inhibition ameliorates periodontitis by reducing oxidative stress and apoptosis via PERK/eIF2 α /ATF-4/CHOP signal pathway in inflammation.

    Techniques Used: Inhibition

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    Cell Signaling Technology Inc perk
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    Cell Signaling Technology Inc endoplasmic reticulum kinase
    Curcumin treatment significantly inhibits the PERK-eIF2 α -ATF4-CHOP signaling pathway and the cleavage of caspase-12. After curcumin treatment (10 μ M) for 48 h, (a) the mRNA levels of GRP78 and CHOP were detected by qRT-PCR, and (b) Western blot was performed to determine the protein levels of GRP78, PERK, p-eIF2 α , eIF2 α , ATF4, CHOP, and cleaved caspase-12. (c) Protein bands of GRP78, PERK, ATF4, CHOP, and cleaved caspase-12 were quantified by densitometry, and relative protein levels were normalized to GAPDH. (d) Protein bands of p-eIF2 α were quantified by densitometry, and relative protein expression of p-eIF2 α was normalized to eIF2 α . Data are shown as the mean ± SD. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001. GRP78: glucose-regulated protein 78; CHOP: C/EBP homologous protein; PERK: protein <t>kinase-like</t> <t>endoplasmic</t> <t>reticulum</t> kinase; eIF2 α : eukaryotic translation initiation factor 2 α ; ATF4: activating transcription factor 4; qRT-PCR: quantitative real-time polymerase chain reaction.
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    Curcumin treatment significantly inhibits the PERK-eIF2 α -ATF4-CHOP signaling pathway and the cleavage of caspase-12. After curcumin treatment (10 μ M) for 48 h, (a) the mRNA levels of GRP78 and CHOP were detected by qRT-PCR, and (b) Western blot was performed to determine the protein levels of GRP78, PERK, p-eIF2 α , eIF2 α , ATF4, CHOP, and cleaved caspase-12. (c) Protein bands of GRP78, PERK, ATF4, CHOP, and cleaved caspase-12 were quantified by densitometry, and relative protein levels were normalized to GAPDH. (d) Protein bands of p-eIF2 α were quantified by densitometry, and relative protein expression of p-eIF2 α was normalized to eIF2 α . Data are shown as the mean ± SD. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001. GRP78: glucose-regulated protein 78; CHOP: C/EBP homologous protein; PERK: protein kinase-like endoplasmic reticulum kinase; eIF2 α : eukaryotic translation initiation factor 2 α ; ATF4: activating transcription factor 4; qRT-PCR: quantitative real-time polymerase chain reaction.

    Journal: Gastroenterology Research and Practice

    Article Title: Curcumin Improves Epithelial Barrier Integrity of Caco-2 Monolayers by Inhibiting Endoplasmic Reticulum Stress and Subsequent Apoptosis

    doi: 10.1155/2021/5570796

    Figure Lengend Snippet: Curcumin treatment significantly inhibits the PERK-eIF2 α -ATF4-CHOP signaling pathway and the cleavage of caspase-12. After curcumin treatment (10 μ M) for 48 h, (a) the mRNA levels of GRP78 and CHOP were detected by qRT-PCR, and (b) Western blot was performed to determine the protein levels of GRP78, PERK, p-eIF2 α , eIF2 α , ATF4, CHOP, and cleaved caspase-12. (c) Protein bands of GRP78, PERK, ATF4, CHOP, and cleaved caspase-12 were quantified by densitometry, and relative protein levels were normalized to GAPDH. (d) Protein bands of p-eIF2 α were quantified by densitometry, and relative protein expression of p-eIF2 α was normalized to eIF2 α . Data are shown as the mean ± SD. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001. GRP78: glucose-regulated protein 78; CHOP: C/EBP homologous protein; PERK: protein kinase-like endoplasmic reticulum kinase; eIF2 α : eukaryotic translation initiation factor 2 α ; ATF4: activating transcription factor 4; qRT-PCR: quantitative real-time polymerase chain reaction.

    Article Snippet: Rabbit antibodies against zonula occludens- (ZO-) 1 (8193), claudin-1 (13255), γ H2AX (Ser139; 9718), glucose-regulated protein 78 (GRP78; 3183), protein kinase-like endoplasmic reticulum kinase (PERK; 5683), eukaryotic translation initiation factor 2 α (eIF2 α ; 5324), p-eIF2 α (3398), activating transcription factor 4 (ATF4; 11815), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH; 2118) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Quantitative RT-PCR, Western Blot, Expressing, Real-time Polymerase Chain Reaction