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Proteintech atf6

ER stress activity is decreased in IMQ-induced psoriatic mice. (a) Representative IHC images of untreated mouse skin and IMQ-induced psoriatic lesions stained for Grp78, XBP1s, and PERK. Expression of ER stress markers was significantly reduced in IMQ-induced psoriasis ( N = 6) versus untreated control group ( N = 6). (b) Correlation analysis between Grp78 and IVL or KRT1 in IMQ-induced psoriatic mice ( N = 6) and untreated mouse skin samples ( N = 6). (c) Reduced ER stress activity correlated with altered keratinocyte differentiation and proliferation in psoriasis. Western blot analysis of IVL, KRT1, Grp78, p-PERK, XBP1s, and <t>ATF6</t> in tissues from IMQ-induced psoriatic ( N = 8) and control mice ( N = 5). Scale bar=100 µm. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Atf6, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 457 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/24169+1+ap/ATF6+Antibody/pmc12997330-141-33-34
Average 96 stars, based on 457 article reviews

atf6 - by Bioz Stars, 2026-09

96/100 stars

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1) Product Images from "Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes"

Article Title: Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes

Journal: Cell Stress & Chaperones

doi: 10.1016/j.cstres.2026.100163

Figure Legend Snippet: ER stress activity is decreased in IMQ-induced psoriatic mice. (a) Representative IHC images of untreated mouse skin and IMQ-induced psoriatic lesions stained for Grp78, XBP1s, and PERK. Expression of ER stress markers was significantly reduced in IMQ-induced psoriasis ( N = 6) versus untreated control group ( N = 6). (b) Correlation analysis between Grp78 and IVL or KRT1 in IMQ-induced psoriatic mice ( N = 6) and untreated mouse skin samples ( N = 6). (c) Reduced ER stress activity correlated with altered keratinocyte differentiation and proliferation in psoriasis. Western blot analysis of IVL, KRT1, Grp78, p-PERK, XBP1s, and ATF6 in tissues from IMQ-induced psoriatic ( N = 8) and control mice ( N = 5). Scale bar=100 µm. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Techniques Used: Activity Assay, Staining, Expressing, Control, Western Blot

ER stress inducers attenuate psoriatic phenotypes via UPR pathways activation. (a) Representative IHC staining for XBP1s and PERK in lesion tissues from IMQ-induced mice with or without ER stress inducer TM/BFA treatment, with corresponding IHC scores. Scale bar=100 µm. (b) Time-course Western blot analysis of IVL, KRT1, Grp78, p-PERK/PERK, XBP1s/XBP1, and ATF6 in primary mouse keratinocytes (mKCs) treated with TM (0.1 μg/mL) or BFA (20 nM) for 0-48 h. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Figure Legend Snippet: ER stress inducers attenuate psoriatic phenotypes via UPR pathways activation. (a) Representative IHC staining for XBP1s and PERK in lesion tissues from IMQ-induced mice with or without ER stress inducer TM/BFA treatment, with corresponding IHC scores. Scale bar=100 µm. (b) Time-course Western blot analysis of IVL, KRT1, Grp78, p-PERK/PERK, XBP1s/XBP1, and ATF6 in primary mouse keratinocytes (mKCs) treated with TM (0.1 μg/mL) or BFA (20 nM) for 0-48 h. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Techniques Used: Activation Assay, Immunohistochemistry, Western Blot

Grp78 synergizes with ER stress inducers to promote keratinocyte differentiation. (a) and (b) Primary mouse keratinocytes were transfected with shRNA against GRP78 (shGrp78-mKCs) or non-targeting control (shnon-mKCs) and treated with TM (0.1 μg/mL) or BFA (20 nM) for 24 and 48 h. Expression of IVL and KRT1, Grp78, p-PERK/PERK, XBP1s/XBP1, and ATF6 was assessed by Western blot. (c) and (d) HaCaT cells expressing shGrp78 (shGrp78-HaCaT) or control shRNA (shnon-HaCaT) were treated similarly, and protein expression was analyzed by Western blot.

Figure Legend Snippet: Grp78 synergizes with ER stress inducers to promote keratinocyte differentiation. (a) and (b) Primary mouse keratinocytes were transfected with shRNA against GRP78 (shGrp78-mKCs) or non-targeting control (shnon-mKCs) and treated with TM (0.1 μg/mL) or BFA (20 nM) for 24 and 48 h. Expression of IVL and KRT1, Grp78, p-PERK/PERK, XBP1s/XBP1, and ATF6 was assessed by Western blot. (c) and (d) HaCaT cells expressing shGrp78 (shGrp78-HaCaT) or control shRNA (shnon-HaCaT) were treated similarly, and protein expression was analyzed by Western blot.

Techniques Used: Transfection, shRNA, Control, Expressing, Western Blot

other:

Article Title: Modulation of the endoplasmic reticulum stress and unfolded protein response mitigates the behavioral effects of early-life stress
Article Snippet: ATF6 , Rabbit , 1:1000 , Proteintech , 24169–1-AP.

Article Title: EETs alleviate alveolar epithelial cell senescence by inhibiting endoplasmic reticulum stress through the Trim25/Keap1/Nrf2 axis
Article Snippet: Anti-ATF6 polyclonal antibody , Proteintech , 24169-1-AP.

Incubation:

Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway
Article Snippet: .. Sections were incubated with anti-ATF6 1:200, 24169-1-AP, Proteintech, Wuhan, China), anti-FHL2 (1:200, 21619-1-AP, Proteintech, Wuhan, China), or anti-TRAF6 (1:200, AF5376, Affinity Biosciences, Zhenjiang, China). .. Detection used IHC reagents (1:100, SPN-9001/SPN-9002, Beijing Zhongshan Golden Bridge Biotechnology Co., Ltd.).

Western Blot:

Article Title: Pathogenic mechanisms of amyotrophic lateral sclerosis-linked VAPB P56S mutation in the degeneration of corticospinal motor neurons
Article Snippet: CHOP , Proteintech , 15204-1-AP , WB. .. ATF6 , Proteintech , 24169-1-AP , WB. ..

Article Title: Role of UPR Sensor Activation in Cell Death–Survival Decision of Colon Cancer Cells Stressed by DPE Treatment
Article Snippet: The gels were transferred to nitrocellulose membranes (Biorad, Hercules) for 1.5 h in Tris–glycine buffer and the membranes were blocked in 1× PBS-0.1% Tween20 solution containing 3% of BSA (Serva), probed with specific antibodies, and developed using ECL Blotting Substrate (Advansta). .. To evaluate protein expression on Western blot membranes, the following antibody were used: rabbit polyclonal anti-ATF6 (1:600) (Proteintech, 24169-1-AP), rabbit polyclonal anti-XBP1 (1:1000) (Novus Biologicals, NB100-80861), rabbit polyclonal anti-phospho-eIF2alpha (Ser51) (1:1000) (Cell Signaling, 9721), rabbit polyclonal anti-eIF2alpha (1:4000) (Cell Signaling, 9722), rabbit polyclonal anti-BiP/GRIP78 (1:5000) (Proteintech, 11587-1-AP), rabbit polyclonal anti-CHOP (GADD153) (1:1000) (Proteintech, 15204-1-AP), mouse monoclonal anti-DUSP5 (1:200) (Santa Cruz Biotechnology Inc., Dallas, TX, USA sc-393801), mouse monoclonal anti-p-ERK (Santa Cruz Biotechnology Inc., sc-7383), rabbit polyclonal anti-ERK1 (Santa Cruz Biotechnology Inc., sc-93), rabbit polyclonal anti-ERK2 (Santa Cruz Biotechnology Inc., sc-154), rabbit monoclonal anti-Mcl1 (1:1000) (Cell Signaling, 39224), mouse monoclonal anti-p53 (1:100) (clone DO-1, Santa Cruz Biotechnology Inc., sc-126). .. Mouse monoclonal anti-β-actin (1:10,000) (Sigma Aldrich) was used as the loading control.

Expressing:

Immunofluorescence:

Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway
Article Snippet: Detection used IHC reagents (1:100, SPN-9001/SPN-9002, Beijing Zhongshan Golden Bridge Biotechnology Co., Ltd.). .. Immunofluorescence was conducted with primary antibodies against ATF6 1:50, 24169-1-AP, Proteintech, Wuhan, China), CD10 (1:50, 18008-1-AP, Proteintech, Wuhan, China), CD31 (1:50, 11265-1-AP, Proteintech, Wuhan, China), FHL2 (1:50, 21619-1-AP, Proteintech, Wuhan, China), or TRAF6 (1:50, AF5376, Affinity Biosciences, Zhenjiang, China). ..

Image Search Results

Journal: Cell Stress & Chaperones

Article Title: Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes

doi: 10.1016/j.cstres.2026.100163

Figure Lengend Snippet: ER stress activity is decreased in IMQ-induced psoriatic mice. (a) Representative IHC images of untreated mouse skin and IMQ-induced psoriatic lesions stained for Grp78, XBP1s, and PERK. Expression of ER stress markers was significantly reduced in IMQ-induced psoriasis ( N = 6) versus untreated control group ( N = 6). (b) Correlation analysis between Grp78 and IVL or KRT1 in IMQ-induced psoriatic mice ( N = 6) and untreated mouse skin samples ( N = 6). (c) Reduced ER stress activity correlated with altered keratinocyte differentiation and proliferation in psoriasis. Western blot analysis of IVL, KRT1, Grp78, p-PERK, XBP1s, and ATF6 in tissues from IMQ-induced psoriatic ( N = 8) and control mice ( N = 5). Scale bar=100 µm. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The following primary antibodies were used for immunoblotting: Grp78 (Santa Cruz, SC-13968), KRT1 (Abclonal, A9776), IVL (Abclonal, A8026), Ki67 (Abcam, ab16667), XBP1s (Abclonal, A17007), XBP1u (Proteintech, 25997-1-AP), PERK (Proteintech, 24390-1-AP), p-PERK (Abclonal, AP1501), ATF6 (Proteintech, 24169-1-AP), β-Actin (Santa Cruz, sc-47778).

Techniques: Activity Assay, Staining, Expressing, Control, Western Blot

Journal: Cell Stress & Chaperones

Article Title: Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes

doi: 10.1016/j.cstres.2026.100163

Figure Lengend Snippet: ER stress inducers attenuate psoriatic phenotypes via UPR pathways activation. (a) Representative IHC staining for XBP1s and PERK in lesion tissues from IMQ-induced mice with or without ER stress inducer TM/BFA treatment, with corresponding IHC scores. Scale bar=100 µm. (b) Time-course Western blot analysis of IVL, KRT1, Grp78, p-PERK/PERK, XBP1s/XBP1, and ATF6 in primary mouse keratinocytes (mKCs) treated with TM (0.1 μg/mL) or BFA (20 nM) for 0-48 h. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Techniques: Activation Assay, Immunohistochemistry, Western Blot

Journal: Cell Stress & Chaperones

Article Title: Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes

doi: 10.1016/j.cstres.2026.100163

Figure Lengend Snippet: Grp78 synergizes with ER stress inducers to promote keratinocyte differentiation. (a) and (b) Primary mouse keratinocytes were transfected with shRNA against GRP78 (shGrp78-mKCs) or non-targeting control (shnon-mKCs) and treated with TM (0.1 μg/mL) or BFA (20 nM) for 24 and 48 h. Expression of IVL and KRT1, Grp78, p-PERK/PERK, XBP1s/XBP1, and ATF6 was assessed by Western blot. (c) and (d) HaCaT cells expressing shGrp78 (shGrp78-HaCaT) or control shRNA (shnon-HaCaT) were treated similarly, and protein expression was analyzed by Western blot.

Techniques: Transfection, shRNA, Control, Expressing, Western Blot

Renal warm I/R injury in mice increases the expression of ATF6 (A) RT-qPCR analysis of ATF6 expression in mouse kidney tissues. (B–C) Representative Western blot images and quantification of ATF6 and activated ATF6 (cATF6) expression in mouse kidney tissues subjected to Sham and ischemia 1h/reperfusion 6h (I/R). (D–E) Representative IHC images and quantification of ATF6 expression in kidney tissues (Scale bars, 100 μm and 50 μm). (F–G) ATF6 expression in cultured HK-2 in response to normoxia and hypoxia/reoxygenation (H/R) treatment was determined by RT-qPCR and Western blot. (H) Quantitative statistical analysis of ATF6 protein. Data represent mean ± SDs, and statistical analysis was performed using t test. (∗ p < 0.05). T-vs-C means IR-vs-Sham.

Journal: iScience

Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway

doi: 10.1016/j.isci.2026.115173

Figure Lengend Snippet: Renal warm I/R injury in mice increases the expression of ATF6 (A) RT-qPCR analysis of ATF6 expression in mouse kidney tissues. (B–C) Representative Western blot images and quantification of ATF6 and activated ATF6 (cATF6) expression in mouse kidney tissues subjected to Sham and ischemia 1h/reperfusion 6h (I/R). (D–E) Representative IHC images and quantification of ATF6 expression in kidney tissues (Scale bars, 100 μm and 50 μm). (F–G) ATF6 expression in cultured HK-2 in response to normoxia and hypoxia/reoxygenation (H/R) treatment was determined by RT-qPCR and Western blot. (H) Quantitative statistical analysis of ATF6 protein. Data represent mean ± SDs, and statistical analysis was performed using t test. (∗ p < 0.05). T-vs-C means IR-vs-Sham.

Article Snippet: Immunofluorescence was conducted with primary antibodies against ATF6 1:50, 24169-1-AP, Proteintech, Wuhan, China), CD10 (1:50, 18008-1-AP, Proteintech, Wuhan, China), CD31 (1:50, 11265-1-AP, Proteintech, Wuhan, China), FHL2 (1:50, 21619-1-AP, Proteintech, Wuhan, China), or TRAF6 (1:50, AF5376, Affinity Biosciences, Zhenjiang, China).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Cell Culture

ATF6 plays a protective role in renal ischemia-reperfusion injury (A–B) The levels of serum Cr and BUN in mice. (C–D) The levels of serum IL-6 and TNF-α in mice. (E–F) The representative images and kidney injury assessment score of HE staining of the kidney. Ceapin-A7 (10 μM) is an ATF6 inhibitor, and AA147 (10 μM) is an ATF6 agonist. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

Journal: iScience

Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway

doi: 10.1016/j.isci.2026.115173

Figure Lengend Snippet: ATF6 plays a protective role in renal ischemia-reperfusion injury (A–B) The levels of serum Cr and BUN in mice. (C–D) The levels of serum IL-6 and TNF-α in mice. (E–F) The representative images and kidney injury assessment score of HE staining of the kidney. Ceapin-A7 (10 μM) is an ATF6 inhibitor, and AA147 (10 μM) is an ATF6 agonist. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

Techniques: Staining

Journal: iScience

Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway

doi: 10.1016/j.isci.2026.115173

Figure Lengend Snippet: ATF6 plays a protective role in renal ischemia-reperfusion injury (A–B) The levels of serum Cr and BUN in mice. (C–D) The levels of serum IL-6 and TNF-α in mice. (E–F) The representative images and kidney injury assessment score of HE staining of the kidney. (G–H) RT-qPCR analysis of TNF-α and IL-6 expression in cultured HK-2 in response to H/R treatment. (I–J) RT-qPCR analysis of IL-6 and TNF-α expression in cultured HK-2 in response to H/R using siATF6. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

Techniques: Staining, Quantitative RT-PCR, Expressing, Cell Culture

ATF6 inhibits the activation of the NF-κB pathway (A) Western blot detection of the expression of NF-κB pathway-related proteins in renal tissue; GAPDH was used as a loading control. (B) Quantitative analysis of protein expression, data represent mean ± SDs, and statistical analysis was performed using t test. (∗ p < 0.05). (C) After hypoxia/reoxygenation in the WT group and knockdown group, the expression of NF-κB pathway-related proteins was detected by Western blot, GAPDH was used as a loading control. (D) Quantitative analysis of protein expression. (E) After hypoxia/reoxygenation in the WT group and the ATF6 overexpression group, the expression of NF-κB pathway-related proteins was detected by Western blot, GAPDH was used as a loading control. (F) Quantitative analysis of protein expression. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

Journal: iScience

Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway

doi: 10.1016/j.isci.2026.115173

Figure Lengend Snippet: ATF6 inhibits the activation of the NF-κB pathway (A) Western blot detection of the expression of NF-κB pathway-related proteins in renal tissue; GAPDH was used as a loading control. (B) Quantitative analysis of protein expression, data represent mean ± SDs, and statistical analysis was performed using t test. (∗ p < 0.05). (C) After hypoxia/reoxygenation in the WT group and knockdown group, the expression of NF-κB pathway-related proteins was detected by Western blot, GAPDH was used as a loading control. (D) Quantitative analysis of protein expression. (E) After hypoxia/reoxygenation in the WT group and the ATF6 overexpression group, the expression of NF-κB pathway-related proteins was detected by Western blot, GAPDH was used as a loading control. (F) Quantitative analysis of protein expression. Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

Techniques: Activation Assay, Western Blot, Expressing, Control, Knockdown, Over Expression

The expression of FHL2 is transcriptionally regulated by ATF6 (A) Expression of FHL2 in RNA-seq after using siATF6. (B) RT-qPCR analysis of FHL2 expression in mouse kidney tissues. (C) Representative Western blot images and quantification of FHL2 expression in mouse kidney tissues (GAPDH as the loading control). (D–E) Representative IHC images and quantification of FHL2 expression in kidney tissues (Scale bars, 100 μm). (F–G) FHL2 expression in cultured HK-2 in response to normoxia and hypoxia/reoxygenation (H/R) treatment was determined by Western blot. GAPDH was used as a loading control. (H–I) The expression of FHL2 and ATF6 in HK-2 cells after ATF6 knockdown was examined by Western blot. GAPDH was used as a loading control; (J-K) The expression of FHL2 and ATF6 in HK-2 cell lines after ATF6 overexpression was examined by Western blot. GAPDH was used as a loading control. (L) The input of ATF6 and IgG binding the FHL2 promoters in HK-2 after hypoxia/physoxia treatment by CHIP-qPCR. (M) Luciferase activity of transfected HEK-293T targeting FHL2 and its mutant after H/R using the dual-luciferase reporter assay. (N) The putative ATF6-binding sites in the FHL2 promoter and the nucleotide sequences representing the predicted binding sequences with the red capital letters indicating core binding elements; Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

Journal: iScience

Article Title: ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway

doi: 10.1016/j.isci.2026.115173

Figure Lengend Snippet: The expression of FHL2 is transcriptionally regulated by ATF6 (A) Expression of FHL2 in RNA-seq after using siATF6. (B) RT-qPCR analysis of FHL2 expression in mouse kidney tissues. (C) Representative Western blot images and quantification of FHL2 expression in mouse kidney tissues (GAPDH as the loading control). (D–E) Representative IHC images and quantification of FHL2 expression in kidney tissues (Scale bars, 100 μm). (F–G) FHL2 expression in cultured HK-2 in response to normoxia and hypoxia/reoxygenation (H/R) treatment was determined by Western blot. GAPDH was used as a loading control. (H–I) The expression of FHL2 and ATF6 in HK-2 cells after ATF6 knockdown was examined by Western blot. GAPDH was used as a loading control; (J-K) The expression of FHL2 and ATF6 in HK-2 cell lines after ATF6 overexpression was examined by Western blot. GAPDH was used as a loading control. (L) The input of ATF6 and IgG binding the FHL2 promoters in HK-2 after hypoxia/physoxia treatment by CHIP-qPCR. (M) Luciferase activity of transfected HEK-293T targeting FHL2 and its mutant after H/R using the dual-luciferase reporter assay. (N) The putative ATF6-binding sites in the FHL2 promoter and the nucleotide sequences representing the predicted binding sequences with the red capital letters indicating core binding elements; Data represent mean ± SDs, and statistical analysis was performed using one-way ANOVA. (∗ p < 0.05).

Techniques: Expressing, RNA Sequencing, Quantitative RT-PCR, Western Blot, Control, Cell Culture, Knockdown, Over Expression, Binding Assay, ChIP-qPCR, Luciferase, Activity Assay, Transfection, Mutagenesis, Reporter Assay

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atf6 (Proteintech)

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