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rat anti grp94 monoclonal antibody (StressMarq)

Name: rat anti grp94 monoclonal antibody
Brand: StressMarq
Rating: 93 (3 reviews)

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StressMarq rat anti grp94 monoclonal antibody
Rat Anti Grp94 Monoclonal Antibody, supplied by StressMarq, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rat anti grp94 monoclonal antibody/product/StressMarq
Average 93 stars, based on 3 article reviews

rat anti grp94 monoclonal antibody - by Bioz Stars, 2026-03

93/100 stars

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gp96 (StressMarq)

StressMarq gp96

HSP90B1 and HSPA5 genes and <t>GP96</t> are induced in ALD. (A) mRNA abundance of HSP90B1 and HSPA5 genes (in transcripts per million) was evaluated by RNA sequencing in patients with normal liver (n = 10), early ASH (n = 12), severe_AH (n = 17), explants_AH (n = 10), and livers from NAFLD (n = 10), HCV (n = 10), and comp_Cirrhosis (n = 9). (B) Representative immunohistochemistry of GP96 in human normal and alcoholic liver (magnification × 200). WT mice were fed with control liquid diet (pair‐fed) or diet containing 5% alcohol for 4 weeks. The mRNA expression of GP96 and GRP78 was measured by RT‐PCR in livers (C) and isolated hepatocytes (E) and liver macrophages (n = 4‐10). (D) Protein level of GP96 and GRP78 in liver lysate was analyzed by western blotting (n = 6). (F) BMDMs were treated with 25 mM ethanol and mRNA expression of GP96 and GRP78 (n = 6). (G) The protein level of GP96 was analyzed at different time intervals (n = 3). Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Abbreviations: EtOH, alcohol; comp, compensated; tpm, transcripts per million.

Gp96, supplied by StressMarq, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/gp96/product/StressMarq
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HSP90B1 and HSPA5 genes and GP96 are induced in ALD. (A) mRNA abundance of HSP90B1 and HSPA5 genes (in transcripts per million) was evaluated by RNA sequencing in patients with normal liver (n = 10), early ASH (n = 12), severe_AH (n = 17), explants_AH (n = 10), and livers from NAFLD (n = 10), HCV (n = 10), and comp_Cirrhosis (n = 9). (B) Representative immunohistochemistry of GP96 in human normal and alcoholic liver (magnification × 200). WT mice were fed with control liquid diet (pair‐fed) or diet containing 5% alcohol for 4 weeks. The mRNA expression of GP96 and GRP78 was measured by RT‐PCR in livers (C) and isolated hepatocytes (E) and liver macrophages (n = 4‐10). (D) Protein level of GP96 and GRP78 in liver lysate was analyzed by western blotting (n = 6). (F) BMDMs were treated with 25 mM ethanol and mRNA expression of GP96 and GRP78 (n = 6). (G) The protein level of GP96 was analyzed at different time intervals (n = 3). Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Abbreviations: EtOH, alcohol; comp, compensated; tpm, transcripts per million.

Journal: Hepatology Communications

Article Title: Myeloid Endoplasmic Reticulum Resident Chaperone GP96 Facilitates Inflammation and Steatosis in Alcohol‐Associated Liver Disease

doi: 10.1002/hep4.1713

Figure Lengend Snippet: HSP90B1 and HSPA5 genes and GP96 are induced in ALD. (A) mRNA abundance of HSP90B1 and HSPA5 genes (in transcripts per million) was evaluated by RNA sequencing in patients with normal liver (n = 10), early ASH (n = 12), severe_AH (n = 17), explants_AH (n = 10), and livers from NAFLD (n = 10), HCV (n = 10), and comp_Cirrhosis (n = 9). (B) Representative immunohistochemistry of GP96 in human normal and alcoholic liver (magnification × 200). WT mice were fed with control liquid diet (pair‐fed) or diet containing 5% alcohol for 4 weeks. The mRNA expression of GP96 and GRP78 was measured by RT‐PCR in livers (C) and isolated hepatocytes (E) and liver macrophages (n = 4‐10). (D) Protein level of GP96 and GRP78 in liver lysate was analyzed by western blotting (n = 6). (F) BMDMs were treated with 25 mM ethanol and mRNA expression of GP96 and GRP78 (n = 6). (G) The protein level of GP96 was analyzed at different time intervals (n = 3). Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Abbreviations: EtOH, alcohol; comp, compensated; tpm, transcripts per million.

Article Snippet: Antibodies used were GP96 (SMC‐105; StressMarq Biosciences, Cadboro, Canada), GRP78 (CST‐3183; Cell Signaling Technology), peroxisome proliferator‐activated receptor alpha (PPAR‐α) (sc‐9000; Santa Cruz Biotechnology, Dallas, TX), CyP2e1 (AB1252; MilliporeSigma, Burlington, MA), calnexin (ab2295; Abcam, Cambridge, United Kingdom), C/EBP‐homologous protein (CHOP) (sc‐7351; Santa Cruz Biotechnology), ATF6α (sc‐166659; Santa Cruz Biotechnology), ATF4 (10835‐1‐AP; Proteintech, Rosemont, IL), ATF3 (sc‐81189; Santa Cruz Biotechnology), β‐actin (ab6276; Abcam), tubulin (ab6046; Abcam), and TATA‐box protein (TBP) (ab818, Abcam).

Techniques: RNA Sequencing Assay, Immunohistochemistry, Expressing, Reverse Transcription Polymerase Chain Reaction, Isolation, Western Blot

Myeloid‐specific GP96 deficiency alleviates chronic alcohol‐induced liver injury. Female WT and M‐GP96KO mice were fed with isocaloric control liquid diet (pair‐fed) or 5% alcohol‐containing Leiber‐DeCarli diet (alcohol‐fed) for 4 weeks, and liver‐to–body weight ratio (A), serum levels of ALT (n = 10‐16) (B), and liver triglycerides (C) were analyzed. Representative photomicrographs of hepatic injury and steatosis assessed by H&E (D) and Oil Red O (E) staining in livers of mice of the indicated genotype (magnification × 100). Percentage of Oil Red O–positive area was quantitated by ImageJ (n = 3‐6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Abbreviations: EtOH, alcohol; wt, weight.

Journal: Hepatology Communications

Article Title: Myeloid Endoplasmic Reticulum Resident Chaperone GP96 Facilitates Inflammation and Steatosis in Alcohol‐Associated Liver Disease

doi: 10.1002/hep4.1713

Figure Lengend Snippet: Myeloid‐specific GP96 deficiency alleviates chronic alcohol‐induced liver injury. Female WT and M‐GP96KO mice were fed with isocaloric control liquid diet (pair‐fed) or 5% alcohol‐containing Leiber‐DeCarli diet (alcohol‐fed) for 4 weeks, and liver‐to–body weight ratio (A), serum levels of ALT (n = 10‐16) (B), and liver triglycerides (C) were analyzed. Representative photomicrographs of hepatic injury and steatosis assessed by H&E (D) and Oil Red O (E) staining in livers of mice of the indicated genotype (magnification × 100). Percentage of Oil Red O–positive area was quantitated by ImageJ (n = 3‐6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Abbreviations: EtOH, alcohol; wt, weight.

Techniques: Staining

Mice lacking myeloid‐specific GP96 exhibit altered lipid metabolism after 4 weeks of alcohol consumption. (A) PPAR‐α protein was detected in nuclear extracts of livers by western blot, and expression was quantitated and normalized to pair‐fed group (n = 4). TBP was used as loading control. The mRNA expression of genes involved in fatty acid β‐oxidation (CPT1a, ACOX1, LCAD, and MCAD) (B‐E) and lipogenesis (SREBPF1, SCD1, and FAS) (F‐H) was analyzed in WT and M‐GP96KO hepatocytes by RT‐PCR and compared with pair‐fed control (n = 3‐6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Hepatology Communications

Article Title: Myeloid Endoplasmic Reticulum Resident Chaperone GP96 Facilitates Inflammation and Steatosis in Alcohol‐Associated Liver Disease

doi: 10.1002/hep4.1713

Figure Lengend Snippet: Mice lacking myeloid‐specific GP96 exhibit altered lipid metabolism after 4 weeks of alcohol consumption. (A) PPAR‐α protein was detected in nuclear extracts of livers by western blot, and expression was quantitated and normalized to pair‐fed group (n = 4). TBP was used as loading control. The mRNA expression of genes involved in fatty acid β‐oxidation (CPT1a, ACOX1, LCAD, and MCAD) (B‐E) and lipogenesis (SREBPF1, SCD1, and FAS) (F‐H) was analyzed in WT and M‐GP96KO hepatocytes by RT‐PCR and compared with pair‐fed control (n = 3‐6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Techniques: Western Blot, Expressing, Reverse Transcription Polymerase Chain Reaction

$Myeloid‐specific GP96 deficiency prevents chronic alcohol‐induced endotoxin and pro‐inflammatory cytokine production. (A) Endotoxin level was measured in serum (n = 8‐12). (B) CyP2e1 was detected in liver microsomal fraction by western blot, and calnexin was used as an internal loading control (n = 3). Total RNA from liver tissue was subjected to quantitative RT‐PCR for analysis of pro‐inflammatory cytokines TNF‐α, IL‐6, MCP‐1, and IL‐1β; NLRP3; anti‐inflammatory markers IL‐10, TGF‐β, and ATF3 (C); and macrophage markers (n = 6‐10) (F). (D) Total liver protein level for TNF‐α was measured in tissue extracts of pair‐fed and alcohol‐fed mice by ELISA (n = 6‐10). (E) ATF3 protein level was analyzed by western blot in whole‐liver extracts using tubulin as an internal control (n = 3). The mRNA expression profile of (G) pro‐inflammatory, and (H) anti‐inflammatory and restorative macrophage markers, Trem2 and ATF3, were analyzed in liver macrophages of pair‐fed and alcohol‐fed mice (n = 5). (I) The mRNA level of pro‐inflammatory cytokines was analyzed in BMDMs isolated from WT and M‐GP96KO mice and stimulated with 100 ng/mL LPS for 2 hours (n = 9). Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.$

Journal: Hepatology Communications

Article Title: Myeloid Endoplasmic Reticulum Resident Chaperone GP96 Facilitates Inflammation and Steatosis in Alcohol‐Associated Liver Disease

doi: 10.1002/hep4.1713

Figure Lengend Snippet: Myeloid‐specific GP96 deficiency prevents chronic alcohol‐induced endotoxin and pro‐inflammatory cytokine production. (A) Endotoxin level was measured in serum (n = 8‐12). (B) CyP2e1 was detected in liver microsomal fraction by western blot, and calnexin was used as an internal loading control (n = 3). Total RNA from liver tissue was subjected to quantitative RT‐PCR for analysis of pro‐inflammatory cytokines TNF‐α, IL‐6, MCP‐1, and IL‐1β; NLRP3; anti‐inflammatory markers IL‐10, TGF‐β, and ATF3 (C); and macrophage markers (n = 6‐10) (F). (D) Total liver protein level for TNF‐α was measured in tissue extracts of pair‐fed and alcohol‐fed mice by ELISA (n = 6‐10). (E) ATF3 protein level was analyzed by western blot in whole‐liver extracts using tubulin as an internal control (n = 3). The mRNA expression profile of (G) pro‐inflammatory, and (H) anti‐inflammatory and restorative macrophage markers, Trem2 and ATF3, were analyzed in liver macrophages of pair‐fed and alcohol‐fed mice (n = 5). (I) The mRNA level of pro‐inflammatory cytokines was analyzed in BMDMs isolated from WT and M‐GP96KO mice and stimulated with 100 ng/mL LPS for 2 hours (n = 9). Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Techniques: Western Blot, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Expressing, Isolation

Loss of myeloid‐specific GP96 prevents LPS‐induced liver injury and inflammation. Female WT and M‐GP96KO mice were injected intraperitoneally with LPS (0.5 mg/kg body weight or saline (n = 4‐8). Serum was collected after 18 hours and subjected to analysis of ALT (A) and AST (B) and compared with the control group. (C) Livers were collected 2 hours after LPS injection, and liver cytokine mRNA was analyzed by RT‐PCR. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, **** P < 0.0001.

Journal: Hepatology Communications

Article Title: Myeloid Endoplasmic Reticulum Resident Chaperone GP96 Facilitates Inflammation and Steatosis in Alcohol‐Associated Liver Disease

doi: 10.1002/hep4.1713

Figure Lengend Snippet: Loss of myeloid‐specific GP96 prevents LPS‐induced liver injury and inflammation. Female WT and M‐GP96KO mice were injected intraperitoneally with LPS (0.5 mg/kg body weight or saline (n = 4‐8). Serum was collected after 18 hours and subjected to analysis of ALT (A) and AST (B) and compared with the control group. (C) Livers were collected 2 hours after LPS injection, and liver cytokine mRNA was analyzed by RT‐PCR. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, **** P < 0.0001.

Techniques: Injection, Reverse Transcription Polymerase Chain Reaction

Inhibition of GP96 using specific inhibitor PU‐WS13 and siRNA reduces LPS‐induced pro‐inflammatory cytokine production. BMDMs were isolated from C57BL/6J mice and stimulated with LPS (100 ng/mL) for 2 hours and treated with PU‐WS13 (0.5 μM) either alone for 2 hours or before LPS for 1 hour. DMSO‐treated cells served as control group (n = 8). RT‐PCR was carried out to evaluate the expression of TNF‐α (A), IL‐6 (B), IL‐1β (C), and MCP‐1 (D) and compared with the untreated group. (E) Culture supernatant was evaluated for secreted TNF‐α by ELISA. (F) Murine macrophage RAW 264.7 cell line was transiently transfected with GP96 siRNA (100 nM) or negative control siRNA for 48 hours and stimulated with LPS for the final 6 hours. Secreted TNF‐α level was measured in culture supernatant by ELISA. Data are presented as mean ± SEM. *** P < 0.001, **** P < 0.0001. Abbreviation: ND, not detected.

Journal: Hepatology Communications

Article Title: Myeloid Endoplasmic Reticulum Resident Chaperone GP96 Facilitates Inflammation and Steatosis in Alcohol‐Associated Liver Disease

doi: 10.1002/hep4.1713

Figure Lengend Snippet: Inhibition of GP96 using specific inhibitor PU‐WS13 and siRNA reduces LPS‐induced pro‐inflammatory cytokine production. BMDMs were isolated from C57BL/6J mice and stimulated with LPS (100 ng/mL) for 2 hours and treated with PU‐WS13 (0.5 μM) either alone for 2 hours or before LPS for 1 hour. DMSO‐treated cells served as control group (n = 8). RT‐PCR was carried out to evaluate the expression of TNF‐α (A), IL‐6 (B), IL‐1β (C), and MCP‐1 (D) and compared with the untreated group. (E) Culture supernatant was evaluated for secreted TNF‐α by ELISA. (F) Murine macrophage RAW 264.7 cell line was transiently transfected with GP96 siRNA (100 nM) or negative control siRNA for 48 hours and stimulated with LPS for the final 6 hours. Secreted TNF‐α level was measured in culture supernatant by ELISA. Data are presented as mean ± SEM. *** P < 0.001, **** P < 0.0001. Abbreviation: ND, not detected.

Techniques: Inhibition, Isolation, Reverse Transcription Polymerase Chain Reaction, Expressing, Enzyme-linked Immunosorbent Assay, Transfection, Negative Control

Schematic representation depicting pathophysiological significance of macrophage‐specific GP96 during chronic alcohol‐mediated liver inflammation and injury.

Journal: Hepatology Communications

Article Title: Myeloid Endoplasmic Reticulum Resident Chaperone GP96 Facilitates Inflammation and Steatosis in Alcohol‐Associated Liver Disease

doi: 10.1002/hep4.1713

Figure Lengend Snippet: Schematic representation depicting pathophysiological significance of macrophage‐specific GP96 during chronic alcohol‐mediated liver inflammation and injury.

Techniques: