total erbb3 d22c5 Search Results


total her3  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc total her3
PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the <t>HER3</t> antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.
Total Her3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+erbb3+d22c5/HER3%2FErbB3+XP+Rabbit+mAb/pmc09838560-98-21-23
Average 96 stars, based on 1 article reviews
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atp5h antibody  (NSJ Bioreagents)
99
NSJ Bioreagents atp5h antibody
PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the <t>HER3</t> antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.
Atp5h Antibody, supplied by NSJ Bioreagents, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+erbb3+d22c5/ATP5H+Antibody/custom%40rq6031%4010%2E1101%2F2024%2E05%2E13%2E594035
Average 99 stars, based on 1 article reviews
atp5h antibody - by Bioz Stars, 2026-09
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total shp2 79  (Becton Dickinson)
90
Becton Dickinson total shp2 79
PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the <t>HER3</t> antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.
Total Shp2 79, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+erbb3+d22c5/anti+shp+2/pmc06050099-194-41-46
Average 90 stars, based on 1 article reviews
total shp2 79 - by Bioz Stars, 2026-09
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total erbb2 42  (Becton Dickinson)
90
Becton Dickinson total erbb2 42
PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the <t>HER3</t> antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.
Total Erbb2 42, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+erbb3+d22c5/antibodies+human+c+myc++c+ha+ras+erbb+2/pmc06050099-194-37-46
Average 90 stars, based on 1 article reviews
total erbb2 42 - by Bioz Stars, 2026-09
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phospho enos  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc phospho enos
PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the <t>HER3</t> antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.
Phospho Enos, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+erbb3+d22c5/Phospho-eNOS+(Ser1177)+Antibody/pmc04824141-160-27-31
Average 96 stars, based on 1 article reviews
phospho enos - by Bioz Stars, 2026-09
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anti akt antibody pan  (Cell Signaling Technology Inc)
99
Cell Signaling Technology Inc anti akt antibody pan
PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the <t>HER3</t> antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.
Anti Akt Antibody Pan, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+erbb3+d22c5/Akt+Antibody/pmc08932670-278-40-78
Average 99 stars, based on 1 article reviews
anti akt antibody pan - by Bioz Stars, 2026-09
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pan c67e7 rabbit monoclonal 4691  (Cell Signaling Technology Inc)
98
Cell Signaling Technology Inc pan c67e7 rabbit monoclonal 4691
PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the <t>HER3</t> antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.
Pan C67e7 Rabbit Monoclonal 4691, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+erbb3+d22c5/Akt+(pan)+Rabbit+mAb/pmc11779641-379-30-73
Average 98 stars, based on 1 article reviews
pan c67e7 rabbit monoclonal 4691 - by Bioz Stars, 2026-09
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akt pan 40d4  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc akt pan 40d4
PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the <t>HER3</t> antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.
Akt Pan 40d4, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+erbb3+d22c5/Akt+(pan)+Mouse+mAb/pmc07922773-88-37-41
Average 96 stars, based on 1 article reviews
akt pan 40d4 - by Bioz Stars, 2026-09
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Image Search Results


PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the HER3 antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.

Journal: Journal of cancer science and clinical therapeutics

Article Title: Liver Endothelium Microenvironment Promotes HER3-mediated Cell Growth in Pancreatic Ductal Adenocarcinoma

doi: 10.26502/jcsct.5079182

Figure Lengend Snippet: PDAC cells were incubated in control PDAC CM or CM from different primary liver ECs (EC-1 or EC-9) either in the presence or the absence of the HER3 antibody seribantumab (250 μg/mL). (A, B) The Western blotting and MTT assay, respectively, show that seribantumab blocked liver EC CM-induced HER3-AKT phosphorylation and cell viability in BxPC-3 and Capan-2 cells (HER3 +ve). (C, D) The Western blotting and MTT assay, respectively, show that seribantumab did not block liver EC CM-induced AKT phosphorylation or cell viability in MIA-PaCa2 and PANC-1 cells (HER3 −ve). For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab.

Article Snippet: Phospho-AKT S473 (Cell Signaling Technology Cat# 9271), total AKT (Cell Signaling Technology Cat# 9272), Phospho-HER3 Y1289 (Cell Signaling Technology Cat# 2842), total HER3 (Cell Signaling Technology Cat# 12708).

Techniques: Incubation, Western Blot, MTT Assay, Blocking Assay

PDAC cells were treated with CM for 30 minutes. (A) The RTK array shows phosphorylation of RTKs in BxPC-3 (upper) or PANC-1 (lower) cells treated by PDAC CM or EC-9 CM, with marked phosphorylation for HER2 (P-HER2), HER3 (P-HER3), and insulin receptor (P-Insulin R). (B) Western blotting shows that CM from ECs (EC-1 or EC-9) increased AKT phosphorylation in all cell lines, but only increased HER2-HER3 phosphorylation in BxPC-3 and Capan-2 cells. Total levels of HER3, HER2, AKT, and β-actin were used as loading controls. Data represent the results of at least three independent experiments.

Journal: Journal of cancer science and clinical therapeutics

Article Title: Liver Endothelium Microenvironment Promotes HER3-mediated Cell Growth in Pancreatic Ductal Adenocarcinoma

doi: 10.26502/jcsct.5079182

Figure Lengend Snippet: PDAC cells were treated with CM for 30 minutes. (A) The RTK array shows phosphorylation of RTKs in BxPC-3 (upper) or PANC-1 (lower) cells treated by PDAC CM or EC-9 CM, with marked phosphorylation for HER2 (P-HER2), HER3 (P-HER3), and insulin receptor (P-Insulin R). (B) Western blotting shows that CM from ECs (EC-1 or EC-9) increased AKT phosphorylation in all cell lines, but only increased HER2-HER3 phosphorylation in BxPC-3 and Capan-2 cells. Total levels of HER3, HER2, AKT, and β-actin were used as loading controls. Data represent the results of at least three independent experiments.

Article Snippet: Phospho-AKT S473 (Cell Signaling Technology Cat# 9271), total AKT (Cell Signaling Technology Cat# 9272), Phospho-HER3 Y1289 (Cell Signaling Technology Cat# 2842), total HER3 (Cell Signaling Technology Cat# 12708).

Techniques: Western Blot

PDAC cells were incubated in control PDAC CM, EC-9 CM, or recombinant human NRG (rhNRG) in PDAC CM. (A) Western blotting shows that HER3 and AKT were activated by EC CM and rhNRG in BxPC-3 and Capan-2 cells (HER3 +ve), and that rhNRG did not activate AKT in MIA-PaCa2 and PANC-1 cells (HER3 −ve). (B) The MTT assay shows that adding different doses of rhNRG in PDAC CM increased the cell viability in BxPC-3 and Capan-2 cells (HER3 +ve), with EC-9 CM as positive control and PDAC CM as negative controls. (C) Western blotting shows that transfecting ECs with NRG-specific siRNA (siNRG) depleted NRGs from EC CM, and that (D) NRG-depleted EC CM did not activate HER3-AKT in BxPC-3 and Capan-2 cells. (E) The MTT assay shows that NRG-depleted EC CM (by NRG-specific siRNAs) attenuated EC-induced PDAC cell viability. For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM.

Journal: Journal of cancer science and clinical therapeutics

Article Title: Liver Endothelium Microenvironment Promotes HER3-mediated Cell Growth in Pancreatic Ductal Adenocarcinoma

doi: 10.26502/jcsct.5079182

Figure Lengend Snippet: PDAC cells were incubated in control PDAC CM, EC-9 CM, or recombinant human NRG (rhNRG) in PDAC CM. (A) Western blotting shows that HER3 and AKT were activated by EC CM and rhNRG in BxPC-3 and Capan-2 cells (HER3 +ve), and that rhNRG did not activate AKT in MIA-PaCa2 and PANC-1 cells (HER3 −ve). (B) The MTT assay shows that adding different doses of rhNRG in PDAC CM increased the cell viability in BxPC-3 and Capan-2 cells (HER3 +ve), with EC-9 CM as positive control and PDAC CM as negative controls. (C) Western blotting shows that transfecting ECs with NRG-specific siRNA (siNRG) depleted NRGs from EC CM, and that (D) NRG-depleted EC CM did not activate HER3-AKT in BxPC-3 and Capan-2 cells. (E) The MTT assay shows that NRG-depleted EC CM (by NRG-specific siRNAs) attenuated EC-induced PDAC cell viability. For Western blotting data, total levels of HER3, AKT, and b-actin were used as loading controls. Data represent the results of at least three independent experiments. For MTT assays, mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM.

Article Snippet: Phospho-AKT S473 (Cell Signaling Technology Cat# 9271), total AKT (Cell Signaling Technology Cat# 9272), Phospho-HER3 Y1289 (Cell Signaling Technology Cat# 2842), total HER3 (Cell Signaling Technology Cat# 12708).

Techniques: Incubation, Recombinant, Western Blot, MTT Assay, Positive Control

BxPC-3 and Capan-2 cells (HER3 +ve) were incubated in control PDAC CM or CM from primary liver ECs (EC-9) either in the presence or the absence of the HER2 antibody trastuzumab (50 μg/mL) or the HER3 antibody seribantumab (250 μg/mL). The MTT assays showed that trastuzumab modestly blocked EC-induced PDAC cell viability, and that seribantumab completely blocked EC-induced PDAC cell viability. The combination of trastuzumab and seribantumab had similar inhibition effect on PDAC cell viability compared to seribantumab alone. Mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab, between adjacent groups. n.s., not statistically significant.

Journal: Journal of cancer science and clinical therapeutics

Article Title: Liver Endothelium Microenvironment Promotes HER3-mediated Cell Growth in Pancreatic Ductal Adenocarcinoma

doi: 10.26502/jcsct.5079182

Figure Lengend Snippet: BxPC-3 and Capan-2 cells (HER3 +ve) were incubated in control PDAC CM or CM from primary liver ECs (EC-9) either in the presence or the absence of the HER2 antibody trastuzumab (50 μg/mL) or the HER3 antibody seribantumab (250 μg/mL). The MTT assays showed that trastuzumab modestly blocked EC-induced PDAC cell viability, and that seribantumab completely blocked EC-induced PDAC cell viability. The combination of trastuzumab and seribantumab had similar inhibition effect on PDAC cell viability compared to seribantumab alone. Mean +/− SEM of at least three experiments, *p<0.01 t-test compared to control groups with PDAC CM without seribantumab, between adjacent groups. n.s., not statistically significant.

Article Snippet: Phospho-AKT S473 (Cell Signaling Technology Cat# 9271), total AKT (Cell Signaling Technology Cat# 9272), Phospho-HER3 Y1289 (Cell Signaling Technology Cat# 2842), total HER3 (Cell Signaling Technology Cat# 12708).

Techniques: Incubation, Inhibition

BxPC-3 cells (HER3 +ve) were implanted subQ. Once tumor sizes were confirmed by a caliper on Day 9, mice were randomized and then treated with CM from BxPC-3 cells (PDAC CM) or liver ECs (EC-9 CM), and with control IgG or seribantumab. (A) Tumor size measurements over time show that EC CM increased tumor growth, and that seribantumab blocked EC CM-induced tumor growth. Mean −/+ SD, *P<0.01 one-way ANOVA test between groups after Day 39. (B, C) Quantification of tumor sizes by a caliper and an image of harvested BxPC-3 xenografts. *P<0.01 one-way ANOVA test. (D) IHC staining and quantification of xenograft sections with Ki-67, phospho-HER3 (P-HER3), and phospho-AKT (P-AKT), and were counter stained with hematoxylin. Scale bars represent 100 μm. Quantifications of the stained sections (n=3 tumors/group) show EC CM increased levels of Ki-67, P-HER3 and P-AKT in BxPC3 xenograft, all of which were significantly decreased by seribantumab. Mean −/+ SD, *P<0.001 one-way ANOVA test.

Journal: Journal of cancer science and clinical therapeutics

Article Title: Liver Endothelium Microenvironment Promotes HER3-mediated Cell Growth in Pancreatic Ductal Adenocarcinoma

doi: 10.26502/jcsct.5079182

Figure Lengend Snippet: BxPC-3 cells (HER3 +ve) were implanted subQ. Once tumor sizes were confirmed by a caliper on Day 9, mice were randomized and then treated with CM from BxPC-3 cells (PDAC CM) or liver ECs (EC-9 CM), and with control IgG or seribantumab. (A) Tumor size measurements over time show that EC CM increased tumor growth, and that seribantumab blocked EC CM-induced tumor growth. Mean −/+ SD, *P<0.01 one-way ANOVA test between groups after Day 39. (B, C) Quantification of tumor sizes by a caliper and an image of harvested BxPC-3 xenografts. *P<0.01 one-way ANOVA test. (D) IHC staining and quantification of xenograft sections with Ki-67, phospho-HER3 (P-HER3), and phospho-AKT (P-AKT), and were counter stained with hematoxylin. Scale bars represent 100 μm. Quantifications of the stained sections (n=3 tumors/group) show EC CM increased levels of Ki-67, P-HER3 and P-AKT in BxPC3 xenograft, all of which were significantly decreased by seribantumab. Mean −/+ SD, *P<0.001 one-way ANOVA test.

Article Snippet: Phospho-AKT S473 (Cell Signaling Technology Cat# 9271), total AKT (Cell Signaling Technology Cat# 9272), Phospho-HER3 Y1289 (Cell Signaling Technology Cat# 2842), total HER3 (Cell Signaling Technology Cat# 12708).

Techniques: Immunohistochemistry, Staining