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p ire1α ser724  (Bioss)


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    Bioss p ire1α ser724
    P Ire1α Ser724, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+ire1%CE%B1+ser724/IRE1+(Ser724)+Polyclonal+Antibody/pm42008177-61-5-11
    Average 94 stars, based on 24 article reviews
    p ire1α ser724 - by Bioz Stars, 2026-08
    94/100 stars

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    Bioss p ire1α
    NHE7 activates ER stress pathways in vitro and in vivo. A WB analysis of ER stress markers (p-PERK, <t>p-IRE1α,</t> ATF6) in Ishikawa, HEC-1-A, and HEC-1-B cells following NHE7 overexpressing. B WB analysis of ER stress markers (p-PERK, p-IRE1α, ATF6) in Ishikawa, HEC-1-A, and HEC-1-B cells following NHE7 knockdown. C IHC staining of p-IRE1α and ATF6 in xenograft tumor tissues with NHE7 overexpression. Scale bars, 50 μm (400 ×) and 100 μm (200 ×). D Correlation analysis between NHE7 and ER stress markers (p-IRE1α, ATF6) in clinical EC samples by IHC. Scale bars, 50 μm (400 ×) and 100 μm (200 ×). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01
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    Bioss 1 ap wb p ire1α bioss bs 16698r wb ihc ki67 abclonal a20018 ihc ldha proteintech
    NHE7 activates ER stress pathways in vitro and in vivo. A WB analysis of ER stress markers (p-PERK, <t>p-IRE1α,</t> ATF6) in Ishikawa, HEC-1-A, and HEC-1-B cells following NHE7 overexpressing. B WB analysis of ER stress markers (p-PERK, p-IRE1α, ATF6) in Ishikawa, HEC-1-A, and HEC-1-B cells following NHE7 knockdown. C IHC staining of p-IRE1α and ATF6 in xenograft tumor tissues with NHE7 overexpression. Scale bars, 50 μm (400 ×) and 100 μm (200 ×). D Correlation analysis between NHE7 and ER stress markers (p-IRE1α, ATF6) in clinical EC samples by IHC. Scale bars, 50 μm (400 ×) and 100 μm (200 ×). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01
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    Novus Biologicals rabbit anti phosphorylated ire1α polyclonal antibody
    Immunohistochemistry staining of phosphorylated <t>IRE1α</t> (pIRE1α) protein in the mandibular first molars. (A) Shown are the representative images of immunohistochemistry staining of pIRE1α protein (signal in brown) in the mandibular first molars of 3-week-old Dspp +/+ , Dspp P19L/+ , and Dspp P19L/P19L mice. Each image in (A) is from the middle region of the crown of a sagittally-sectioned mandibular first molar. (A1-A3) are the higher magnification views of the roof-forming odontoblasts (box1), dental pulp cells (box 2) and floor-forming odontoblasts (box 3) in the corresponding images in (A) , respectively. rd, roof dentin; fd, floor dentin; rod, roof-forming odontoblasts; fod, floor-forming odontoblasts; Scale bars: 50 μm in A; 20 μm in (A1-A3). Three independent experiments for IHC staining of pIRE1α show similar results.
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    Novus Biologicals phospho ire1α p ire1α nb100 2323 antibodies
    Immunohistochemistry staining of phosphorylated <t>IRE1α</t> (pIRE1α) protein in the mandibular first molars. (A) Shown are the representative images of immunohistochemistry staining of pIRE1α protein (signal in brown) in the mandibular first molars of 3-week-old Dspp +/+ , Dspp P19L/+ , and Dspp P19L/P19L mice. Each image in (A) is from the middle region of the crown of a sagittally-sectioned mandibular first molar. (A1-A3) are the higher magnification views of the roof-forming odontoblasts (box1), dental pulp cells (box 2) and floor-forming odontoblasts (box 3) in the corresponding images in (A) , respectively. rd, roof dentin; fd, floor dentin; rod, roof-forming odontoblasts; fod, floor-forming odontoblasts; Scale bars: 50 μm in A; 20 μm in (A1-A3). Three independent experiments for IHC staining of pIRE1α show similar results.
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    Image Search Results


    NHE7 activates ER stress pathways in vitro and in vivo. A WB analysis of ER stress markers (p-PERK, p-IRE1α, ATF6) in Ishikawa, HEC-1-A, and HEC-1-B cells following NHE7 overexpressing. B WB analysis of ER stress markers (p-PERK, p-IRE1α, ATF6) in Ishikawa, HEC-1-A, and HEC-1-B cells following NHE7 knockdown. C IHC staining of p-IRE1α and ATF6 in xenograft tumor tissues with NHE7 overexpression. Scale bars, 50 μm (400 ×) and 100 μm (200 ×). D Correlation analysis between NHE7 and ER stress markers (p-IRE1α, ATF6) in clinical EC samples by IHC. Scale bars, 50 μm (400 ×) and 100 μm (200 ×). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01

    Journal: Apoptosis

    Article Title: Hypoxic glycolysis-driven histone lactylation activates NHE7 to promote endometrial cancer progression via COX6C-mediated endoplasmic reticulum stress

    doi: 10.1007/s10495-026-02262-w

    Figure Lengend Snippet: NHE7 activates ER stress pathways in vitro and in vivo. A WB analysis of ER stress markers (p-PERK, p-IRE1α, ATF6) in Ishikawa, HEC-1-A, and HEC-1-B cells following NHE7 overexpressing. B WB analysis of ER stress markers (p-PERK, p-IRE1α, ATF6) in Ishikawa, HEC-1-A, and HEC-1-B cells following NHE7 knockdown. C IHC staining of p-IRE1α and ATF6 in xenograft tumor tissues with NHE7 overexpression. Scale bars, 50 μm (400 ×) and 100 μm (200 ×). D Correlation analysis between NHE7 and ER stress markers (p-IRE1α, ATF6) in clinical EC samples by IHC. Scale bars, 50 μm (400 ×) and 100 μm (200 ×). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01

    Article Snippet: p-IRE1α , BIOSS , bs-16698R , WB/IHC.

    Techniques: In Vitro, In Vivo, Knockdown, Immunohistochemistry, Over Expression

    NHE7 enhances malignant phenotypes and stemness in EC cells by activating the ER stress pathway. A MTT assays were performed to evaluate the effect of 4-PBA concentration on cell viability in Ishikawa cells. Ishikawa cells were divided into pCDH + Control, NHE7 + control and NHE7 + 4-PBA (ER stress inhibitor). B The expressions of p-IRE1α, IRE1α and ATF6 were examined in Ishikawa cells through western blot assay. C The proliferation ability of Ishikawa cells was detected using the MTT assay. D The apoptosis levels of Ishikawa cells were detected using flow cytometry. E The expressions of apoptosis-related markers (cleaved PARP and cleaved Caspase-3) in Ishikawa cells were detected by WB assay. F The colony-forming capacity of Ishikawa cells was tested using a colony formation assay. G The migration and invasion abilities of Ishikawa cells were detected through transwell experiments. Scale bars, 100 μm (100 ×). H Tumor sphere-forming assay showed the effects of NHE7 overexpression and 4-PBA on the tumor sphere formation of Ishikawa cells. I WB analysis assessed the expression levels of EMT markers (E-cadherin, N-cadherin, and Vimentin) and stemness-associated proteins (OCT4, Nanog, and SOX2). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05, ** P < 0.01

    Journal: Apoptosis

    Article Title: Hypoxic glycolysis-driven histone lactylation activates NHE7 to promote endometrial cancer progression via COX6C-mediated endoplasmic reticulum stress

    doi: 10.1007/s10495-026-02262-w

    Figure Lengend Snippet: NHE7 enhances malignant phenotypes and stemness in EC cells by activating the ER stress pathway. A MTT assays were performed to evaluate the effect of 4-PBA concentration on cell viability in Ishikawa cells. Ishikawa cells were divided into pCDH + Control, NHE7 + control and NHE7 + 4-PBA (ER stress inhibitor). B The expressions of p-IRE1α, IRE1α and ATF6 were examined in Ishikawa cells through western blot assay. C The proliferation ability of Ishikawa cells was detected using the MTT assay. D The apoptosis levels of Ishikawa cells were detected using flow cytometry. E The expressions of apoptosis-related markers (cleaved PARP and cleaved Caspase-3) in Ishikawa cells were detected by WB assay. F The colony-forming capacity of Ishikawa cells was tested using a colony formation assay. G The migration and invasion abilities of Ishikawa cells were detected through transwell experiments. Scale bars, 100 μm (100 ×). H Tumor sphere-forming assay showed the effects of NHE7 overexpression and 4-PBA on the tumor sphere formation of Ishikawa cells. I WB analysis assessed the expression levels of EMT markers (E-cadherin, N-cadherin, and Vimentin) and stemness-associated proteins (OCT4, Nanog, and SOX2). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05, ** P < 0.01

    Article Snippet: p-IRE1α , BIOSS , bs-16698R , WB/IHC.

    Techniques: Concentration Assay, Control, Western Blot, MTT Assay, Flow Cytometry, Colony Assay, Migration, Over Expression, Expressing

    NHE7 enhances OXPHOS-induced ER stress by upregulating COX6C expression in EC cells. A WB was used to detect the transfection efficiency of COX6C knockdown in Ishikawa cells. B WB was used to analyze the expression of NHE7 and COX6C in Ishikawa cells after COX6C silencing combined with NHE7 overexpression. C ELISA was used to determine the level of ATP. D Intracellular ROS levels were detected by flow cytometry. E The expression levels of p-IRE1α, IRE1α, and ATF6 were examined in Ishikawa cells. F The apoptosis levels of Ishikawa cells were detected using flow cytometry. G The expressions of apoptosis-related markers (cleaved PARP and cleaved Caspase-3) in Ishikawa cells were detected by WB assay. H The colony-forming capacity of Ishikawa cells was tested by colony formation assay. I The migration and invasion abilities of Ishikawa cells were detected through transwell experiments. Scale bar, 100 μm (100 ×). J Tumor sphere-forming assay showed the effects on the tumor sphere formation of Ishikawa cells. At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01

    Journal: Apoptosis

    Article Title: Hypoxic glycolysis-driven histone lactylation activates NHE7 to promote endometrial cancer progression via COX6C-mediated endoplasmic reticulum stress

    doi: 10.1007/s10495-026-02262-w

    Figure Lengend Snippet: NHE7 enhances OXPHOS-induced ER stress by upregulating COX6C expression in EC cells. A WB was used to detect the transfection efficiency of COX6C knockdown in Ishikawa cells. B WB was used to analyze the expression of NHE7 and COX6C in Ishikawa cells after COX6C silencing combined with NHE7 overexpression. C ELISA was used to determine the level of ATP. D Intracellular ROS levels were detected by flow cytometry. E The expression levels of p-IRE1α, IRE1α, and ATF6 were examined in Ishikawa cells. F The apoptosis levels of Ishikawa cells were detected using flow cytometry. G The expressions of apoptosis-related markers (cleaved PARP and cleaved Caspase-3) in Ishikawa cells were detected by WB assay. H The colony-forming capacity of Ishikawa cells was tested by colony formation assay. I The migration and invasion abilities of Ishikawa cells were detected through transwell experiments. Scale bar, 100 μm (100 ×). J Tumor sphere-forming assay showed the effects on the tumor sphere formation of Ishikawa cells. At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01

    Article Snippet: p-IRE1α , BIOSS , bs-16698R , WB/IHC.

    Techniques: Expressing, Transfection, Knockdown, Over Expression, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Colony Assay, Migration

    COX6C triggers ER stress and enhances the malignant phenotypes of EC cells by upregulating ROS levels. A Intracellular ROS levels were detected by flow cytometry in Ishikawa cells with COX6C overexpression combined with the antioxidant N-acetylcysteine (NAC). B The expression levels of p-IRE1α, IRE1α, and ATF6 were examined in Ishikawa cells. C The proliferation ability of Ishikawa cells was detected using the MTT assay. D The apoptosis levels of Ishikawa cells were detected using flow cytometry. E The expressions of apoptosis-related markers (cleaved PARP and cleaved Caspase-3) in Ishikawa cells were detected by WB assay. F The colony-forming capacity of Ishikawa cells was tested by colony formation assay. G The migration and invasion abilities of Ishikawa cells were detected through transwell experiments. Scale bar, 100 μm (100 ×). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01

    Journal: Apoptosis

    Article Title: Hypoxic glycolysis-driven histone lactylation activates NHE7 to promote endometrial cancer progression via COX6C-mediated endoplasmic reticulum stress

    doi: 10.1007/s10495-026-02262-w

    Figure Lengend Snippet: COX6C triggers ER stress and enhances the malignant phenotypes of EC cells by upregulating ROS levels. A Intracellular ROS levels were detected by flow cytometry in Ishikawa cells with COX6C overexpression combined with the antioxidant N-acetylcysteine (NAC). B The expression levels of p-IRE1α, IRE1α, and ATF6 were examined in Ishikawa cells. C The proliferation ability of Ishikawa cells was detected using the MTT assay. D The apoptosis levels of Ishikawa cells were detected using flow cytometry. E The expressions of apoptosis-related markers (cleaved PARP and cleaved Caspase-3) in Ishikawa cells were detected by WB assay. F The colony-forming capacity of Ishikawa cells was tested by colony formation assay. G The migration and invasion abilities of Ishikawa cells were detected through transwell experiments. Scale bar, 100 μm (100 ×). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01

    Article Snippet: p-IRE1α , BIOSS , bs-16698R , WB/IHC.

    Techniques: Flow Cytometry, Over Expression, Expressing, MTT Assay, Colony Assay, Migration

    NHE7 facilitates EC tumor growth by upregulating COX6C expression in vivo. A WB analysis was used to detect the protein expression levels of NHE7 and COX6C in Ishikawa cells overexpressing NHE7, and in Ishikawa cells with concurrent NHE7 overexpression and COX6C knockdown. B Stable Ishikawa cell lines were established for the following conditions: NHE7 overexpression alone, and concurrent NHE7 overexpression with COX6C knockdown, along with their respective control cells. A xenograft tumor model was then generated using these cells. C Tumor growth was monitored and recorded, and D tumor weight was measured at the endpoint. E WB assay was performed to assess the effects of NHE7 overexpression alone or in combination with COX6C knockdown on the levels of apoptosis markers c-PARP and C-Caspase3 in xenograft tumor tissues. F HE staining was performed to assess histopathological damage in xenograft tumor tissues following NHE7 overexpression, either alone or in combination with COX6C knockdown. IHC was performed to evaluate the impact of NHE7 overexpression, either alone or in combination with COX6C knockdown, on the expression of Ki67, E-cadherin, N-cadherin, Vimentin, OCT4, Nanog, SOX2, p-IRE1α, IRE1α, and ATF6 in xenograft tumor tissues. Scale bar, 50 μm (400 ×) and 100 μm (200 ×). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01

    Journal: Apoptosis

    Article Title: Hypoxic glycolysis-driven histone lactylation activates NHE7 to promote endometrial cancer progression via COX6C-mediated endoplasmic reticulum stress

    doi: 10.1007/s10495-026-02262-w

    Figure Lengend Snippet: NHE7 facilitates EC tumor growth by upregulating COX6C expression in vivo. A WB analysis was used to detect the protein expression levels of NHE7 and COX6C in Ishikawa cells overexpressing NHE7, and in Ishikawa cells with concurrent NHE7 overexpression and COX6C knockdown. B Stable Ishikawa cell lines were established for the following conditions: NHE7 overexpression alone, and concurrent NHE7 overexpression with COX6C knockdown, along with their respective control cells. A xenograft tumor model was then generated using these cells. C Tumor growth was monitored and recorded, and D tumor weight was measured at the endpoint. E WB assay was performed to assess the effects of NHE7 overexpression alone or in combination with COX6C knockdown on the levels of apoptosis markers c-PARP and C-Caspase3 in xenograft tumor tissues. F HE staining was performed to assess histopathological damage in xenograft tumor tissues following NHE7 overexpression, either alone or in combination with COX6C knockdown. IHC was performed to evaluate the impact of NHE7 overexpression, either alone or in combination with COX6C knockdown, on the expression of Ki67, E-cadherin, N-cadherin, Vimentin, OCT4, Nanog, SOX2, p-IRE1α, IRE1α, and ATF6 in xenograft tumor tissues. Scale bar, 50 μm (400 ×) and 100 μm (200 ×). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01

    Article Snippet: p-IRE1α , BIOSS , bs-16698R , WB/IHC.

    Techniques: Expressing, In Vivo, Over Expression, Knockdown, Control, Generated, Staining

    Immunohistochemistry staining of phosphorylated IRE1α (pIRE1α) protein in the mandibular first molars. (A) Shown are the representative images of immunohistochemistry staining of pIRE1α protein (signal in brown) in the mandibular first molars of 3-week-old Dspp +/+ , Dspp P19L/+ , and Dspp P19L/P19L mice. Each image in (A) is from the middle region of the crown of a sagittally-sectioned mandibular first molar. (A1-A3) are the higher magnification views of the roof-forming odontoblasts (box1), dental pulp cells (box 2) and floor-forming odontoblasts (box 3) in the corresponding images in (A) , respectively. rd, roof dentin; fd, floor dentin; rod, roof-forming odontoblasts; fod, floor-forming odontoblasts; Scale bars: 50 μm in A; 20 μm in (A1-A3). Three independent experiments for IHC staining of pIRE1α show similar results.

    Journal: Frontiers in Physiology

    Article Title: Inositol-requiring enzyme 1 alpha is essential for dentinogenesis

    doi: 10.3389/fphys.2025.1722417

    Figure Lengend Snippet: Immunohistochemistry staining of phosphorylated IRE1α (pIRE1α) protein in the mandibular first molars. (A) Shown are the representative images of immunohistochemistry staining of pIRE1α protein (signal in brown) in the mandibular first molars of 3-week-old Dspp +/+ , Dspp P19L/+ , and Dspp P19L/P19L mice. Each image in (A) is from the middle region of the crown of a sagittally-sectioned mandibular first molar. (A1-A3) are the higher magnification views of the roof-forming odontoblasts (box1), dental pulp cells (box 2) and floor-forming odontoblasts (box 3) in the corresponding images in (A) , respectively. rd, roof dentin; fd, floor dentin; rod, roof-forming odontoblasts; fod, floor-forming odontoblasts; Scale bars: 50 μm in A; 20 μm in (A1-A3). Three independent experiments for IHC staining of pIRE1α show similar results.

    Article Snippet: The primary antibodies used in this study included: 1) rabbit anti-phosphorylated IRE1α polyclonal antibody (1:400, Novus Biologicals, NB100-2323); 2) rabbit anti-XBP1 polyclonal antibody that recognizes both unspliced XBP1 (XBP1U) and spliced XBP1 (XBP1S) (1:200, Abcam, ab37152); 3) rabbit anti-XBP1S monoclonal antibody (E9V3E) that specifically recognizes XBP1S ( ; ) (1:50, Cell Signaling Technology, Danvers, MA); 4) rabbit anti-DSPP polyclonal antibody that recognizes both DSP and full-length DSPP (1:2000) ( ); and 5) rabbit anti-DMP1 polyclonal antibody (1:800, #857) ( ).

    Techniques: Immunohistochemistry, Staining