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MyBiosource Biotechnology human ar elisa kit
Human Ar Elisa Kit, supplied by MyBiosource Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews

human ar elisa kit - by Bioz Stars, 2026-03

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ERBB and MAPK signaling pathway gene expression are up-regulated in vascular endothelial cells (VECs) with Piezo1 activated by Yoda1. (A) Volcano plot of differentially expressed genes in HUVEC and SK-Hep1 cells between treated with the Yoda1 and DMSO (FC > 1.5, P < 0.05). (B) Signal pathway from results of KEGG enrichment analysis based on differential up-regulated genes of HUVEC and SK-Hep1 cells after treatment with Yoda1 vs . DMSO ( P < 0.05). (C) Signal pathway obtained by KEGG enrichment analysis based on the overlap of genes in the ligand library and up-regulated genes in HUVEC and SK-Hep1 cell lines ( P < 0.05). The ligand library is from the CellTalkDB website ( http://tcm.zju.edu.cn/celltalkdb/download.php ). (D) Gene set enrichment analysis suggested that the ERBB signal pathway genes were up-regulated in HUVEC and SK-Hep1 cell lines after Yoda1 activates Piezo1. (E) HBEGF, EREG, AREG, and neuregulin 1 (NRG1) expression were elevated in both HUVEC and SK-Hep1 cells with Piezo1 activated by Yoda1.

Journal: Genes & Diseases

Article Title: EGFR-mediated crosstalk between vascular endothelial cells and hepatocytes promotes Piezo1-dependent liver regeneration

doi: 10.1016/j.gendis.2024.101321

Figure Lengend Snippet: ERBB and MAPK signaling pathway gene expression are up-regulated in vascular endothelial cells (VECs) with Piezo1 activated by Yoda1. (A) Volcano plot of differentially expressed genes in HUVEC and SK-Hep1 cells between treated with the Yoda1 and DMSO (FC > 1.5, P < 0.05). (B) Signal pathway from results of KEGG enrichment analysis based on differential up-regulated genes of HUVEC and SK-Hep1 cells after treatment with Yoda1 vs . DMSO ( P < 0.05). (C) Signal pathway obtained by KEGG enrichment analysis based on the overlap of genes in the ligand library and up-regulated genes in HUVEC and SK-Hep1 cell lines ( P < 0.05). The ligand library is from the CellTalkDB website ( http://tcm.zju.edu.cn/celltalkdb/download.php ). (D) Gene set enrichment analysis suggested that the ERBB signal pathway genes were up-regulated in HUVEC and SK-Hep1 cell lines after Yoda1 activates Piezo1. (E) HBEGF, EREG, AREG, and neuregulin 1 (NRG1) expression were elevated in both HUVEC and SK-Hep1 cells with Piezo1 activated by Yoda1.

Article Snippet: Levels of AREG and EREG were measured using AREG (EK0304) and EREG (EK1394) ELISA kits from Boster Biological Technology (Wuhan, China) following the manufacturer's protocol.

Techniques: Gene Expression, Expressing

Expression of HBEGF, EREG, and AREG induced by Piezo1 activation in vascular endothelial cells (VECs) depends on PKC/ERK1/2 signaling pathways. (A, B) The qRT-PCR results showed increased mRNA expression of HBEGF, EREG, and AREG induced by Yoda1 in endothelial cells and was reversed with Piezo1 knockdown in HUVEC cells. (C, D) the ELISA assay results showed that increased secretion of EREG and AREG in HCMYoda1 were reversed with Piezo1 knockdown. (E) The qRT-PCR results showed the block effect of ravoxertinib (ERK1/2 inhibitor, 5 μM), adezmapimod SB 203580 (P38 MAPK inhibitor, 10 μM), SP (c-Jun N-terminal kinase inhibitor, 25 μM), and SR11302 (activator protein-1 inhibitor, 10 μM) on the expression of HBEGF, EREG, and AREG induced by Yoda1 in HUVEC and SK-Hep1 cells. (F) WB suggests that the knockdown of Piezo1 can inhibit the activation of ERK1/2 induced by Yoda1. (G, H) The WB and qRT-PCR results for non-selective protein kinase inhibitor AM2282 (200 nM) effect on activation of ERK1/2 and the expression of HBEGF, AREG, and EREG in HUVEC cells induced by Yoda1. (I, J) WB and qRT-PCR confirmed that selective protein kinase C inhibitor GO 6983 (10 μM) could inhibit the activation of ERK1/2 and the expression of HBEGF, AREG, and EREG in endothelial cells induced by Yoda1. (K) Immunofluorescence analysis revealed that Yoda1 (5 μM for 0, 5, and 10 min) could activate PKCα. (L) The schematic diagram delineating the probable mechanism of the expression of HBEGF, EREG, and AREG induced by Piezo1 activated by Yoda1. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests. PVEC, mouse primary vascular endothelial cell; HCMYoda1, conditioned medium from HUVEC with Yoda1-activated Piezo1.

Journal: Genes & Diseases

Article Title: EGFR-mediated crosstalk between vascular endothelial cells and hepatocytes promotes Piezo1-dependent liver regeneration

doi: 10.1016/j.gendis.2024.101321

Figure Lengend Snippet: Expression of HBEGF, EREG, and AREG induced by Piezo1 activation in vascular endothelial cells (VECs) depends on PKC/ERK1/2 signaling pathways. (A, B) The qRT-PCR results showed increased mRNA expression of HBEGF, EREG, and AREG induced by Yoda1 in endothelial cells and was reversed with Piezo1 knockdown in HUVEC cells. (C, D) the ELISA assay results showed that increased secretion of EREG and AREG in HCMYoda1 were reversed with Piezo1 knockdown. (E) The qRT-PCR results showed the block effect of ravoxertinib (ERK1/2 inhibitor, 5 μM), adezmapimod SB 203580 (P38 MAPK inhibitor, 10 μM), SP (c-Jun N-terminal kinase inhibitor, 25 μM), and SR11302 (activator protein-1 inhibitor, 10 μM) on the expression of HBEGF, EREG, and AREG induced by Yoda1 in HUVEC and SK-Hep1 cells. (F) WB suggests that the knockdown of Piezo1 can inhibit the activation of ERK1/2 induced by Yoda1. (G, H) The WB and qRT-PCR results for non-selective protein kinase inhibitor AM2282 (200 nM) effect on activation of ERK1/2 and the expression of HBEGF, AREG, and EREG in HUVEC cells induced by Yoda1. (I, J) WB and qRT-PCR confirmed that selective protein kinase C inhibitor GO 6983 (10 μM) could inhibit the activation of ERK1/2 and the expression of HBEGF, AREG, and EREG in endothelial cells induced by Yoda1. (K) Immunofluorescence analysis revealed that Yoda1 (5 μM for 0, 5, and 10 min) could activate PKCα. (L) The schematic diagram delineating the probable mechanism of the expression of HBEGF, EREG, and AREG induced by Piezo1 activated by Yoda1. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests. PVEC, mouse primary vascular endothelial cell; HCMYoda1, conditioned medium from HUVEC with Yoda1-activated Piezo1.

Article Snippet: Levels of AREG and EREG were measured using AREG (EK0304) and EREG (EK1394) ELISA kits from Boster Biological Technology (Wuhan, China) following the manufacturer's protocol.

Techniques: Expressing, Activation Assay, Protein-Protein interactions, Quantitative RT-PCR, Knockdown, Enzyme-linked Immunosorbent Assay, Blocking Assay, Immunofluorescence, Two Tailed Test

AREG and EREG from vascular endothelial cells (VECs) promote hepatocyte proliferation and partial epithelial–mesenchymal transition through the EGFR signal pathway. (A) WB revealed that EGFR was activated following treatment with HCMYoda1 and SCMYoda1. (B) The MTT assay during 48 h proved that gefitinib could block the proliferation of hepatocytes induced by HCMYoda1 and SCMYoda1. (C) The crystal violet staining demonstrated that the morphological changes of hepatocytes induced by HCMYoda1 were inhibited by gefitinib. (D) qRT-PCR analysis suggested that Gefitinib reversed the reduction of cadherin 1 (CDH1) induced by HCMYoda1 but had no significant effect on vimentin (VIM). (E) The MTT assay during 72 h confirmed that the recombinant proteins of AREG and EREG could promote the proliferation of hepatocytes (the results of statistical analysis were obtained by comparing with the Ctrl group). (F) qRT-PCR analysis proved that AREG and EREG promoted partial epithelial–mesenchymal transition of hepatocytes. (G) Differences in basal expression levels of HBEGF, AREG, EREG, CDH1, cadherin 2 (CDH2), and VIM between LO2 and HepaRG cells. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests. HCMYoda1, conditioned medium from HUVEC with Yoda1-activated Piezo1; SCMYoda1, conditioned medium from SK-Hep1 with Yoda1-activated Piezo1.

Journal: Genes & Diseases

Article Title: EGFR-mediated crosstalk between vascular endothelial cells and hepatocytes promotes Piezo1-dependent liver regeneration

doi: 10.1016/j.gendis.2024.101321

Figure Lengend Snippet: AREG and EREG from vascular endothelial cells (VECs) promote hepatocyte proliferation and partial epithelial–mesenchymal transition through the EGFR signal pathway. (A) WB revealed that EGFR was activated following treatment with HCMYoda1 and SCMYoda1. (B) The MTT assay during 48 h proved that gefitinib could block the proliferation of hepatocytes induced by HCMYoda1 and SCMYoda1. (C) The crystal violet staining demonstrated that the morphological changes of hepatocytes induced by HCMYoda1 were inhibited by gefitinib. (D) qRT-PCR analysis suggested that Gefitinib reversed the reduction of cadherin 1 (CDH1) induced by HCMYoda1 but had no significant effect on vimentin (VIM). (E) The MTT assay during 72 h confirmed that the recombinant proteins of AREG and EREG could promote the proliferation of hepatocytes (the results of statistical analysis were obtained by comparing with the Ctrl group). (F) qRT-PCR analysis proved that AREG and EREG promoted partial epithelial–mesenchymal transition of hepatocytes. (G) Differences in basal expression levels of HBEGF, AREG, EREG, CDH1, cadherin 2 (CDH2), and VIM between LO2 and HepaRG cells. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests. HCMYoda1, conditioned medium from HUVEC with Yoda1-activated Piezo1; SCMYoda1, conditioned medium from SK-Hep1 with Yoda1-activated Piezo1.

Article Snippet: Levels of AREG and EREG were measured using AREG (EK0304) and EREG (EK1394) ELISA kits from Boster Biological Technology (Wuhan, China) following the manufacturer's protocol.

Techniques: MTT Assay, Blocking Assay, Staining, Quantitative RT-PCR, Recombinant, Expressing, Two Tailed Test

AREG and EREG promote the proliferation and epithelial–mesenchymal transition of mouse primary hepatocytes in vitro . (A) MTT assay showed that AREG and EREG promoted the proliferation of mouse primary hepatocytes. (B, C) EDU detected that AREG and EREG promoted the proliferation of mouse primary hepatocytes. (D, E) Immunofluorescence assay showed that AREG and EREG promoted the expression of Ki67 in mouse primary hepatocytes. (F) WB detected that AREG and EREG promoted the expression of CyclinD1 in mouse primary hepatocytes. (G) AREG and EREG promoted the morphological changes of mouse primary hepatocytes. (H) The results of qRT-PCR showed that AREG and EREG promoted the down-regulation of cadherin 1 (CDH1) expression and up-regulation of vimentin (VIM) expression in mouse primary hepatocytes. (I) WB showed that AREG and EREG promoted the decrease of E-cadherin expression and the increase of VIM expression. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests. E-cad, E-cadherin.

Journal: Genes & Diseases

Article Title: EGFR-mediated crosstalk between vascular endothelial cells and hepatocytes promotes Piezo1-dependent liver regeneration

doi: 10.1016/j.gendis.2024.101321

Figure Lengend Snippet: AREG and EREG promote the proliferation and epithelial–mesenchymal transition of mouse primary hepatocytes in vitro . (A) MTT assay showed that AREG and EREG promoted the proliferation of mouse primary hepatocytes. (B, C) EDU detected that AREG and EREG promoted the proliferation of mouse primary hepatocytes. (D, E) Immunofluorescence assay showed that AREG and EREG promoted the expression of Ki67 in mouse primary hepatocytes. (F) WB detected that AREG and EREG promoted the expression of CyclinD1 in mouse primary hepatocytes. (G) AREG and EREG promoted the morphological changes of mouse primary hepatocytes. (H) The results of qRT-PCR showed that AREG and EREG promoted the down-regulation of cadherin 1 (CDH1) expression and up-regulation of vimentin (VIM) expression in mouse primary hepatocytes. (I) WB showed that AREG and EREG promoted the decrease of E-cadherin expression and the increase of VIM expression. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests. E-cad, E-cadherin.

Article Snippet: Levels of AREG and EREG were measured using AREG (EK0304) and EREG (EK1394) ELISA kits from Boster Biological Technology (Wuhan, China) following the manufacturer's protocol.

Techniques: In Vitro, MTT Assay, Immunofluorescence, Expressing, Quantitative RT-PCR, Two Tailed Test

EGFR mediates hepatocyte proliferation and liver regeneration. (A) WB revealed that EGFR was activated by recombinant proteins of AREG (50 ng/mL) and EREG (20 ng/mL) in LO2 cells. (B) The MTT assay at 24 and 48 h suggested that gefitinib could block the proliferation of hepatocytes induced by AREG (50 ng/mL) and EREG (20 ng/mL) in LO2 cells (the results of statistical analysis were obtained by comparing with the 0 μM Gef group, respectively). (C) WB demonstrated that ERK1/2 was activated by recombinant proteins of AREG (50 ng/mL) and EREG (20 ng/mL) in LO2 cells. (D) The MTT assay confirmed that the proliferation of LO2 cells induced by AREG and EREG was partially reversed by ravoxertinib (ERK1/2 inhibitor) (the results of statistical analysis were obtained by comparing with the AREG+DMSO group). (E) WB indicated that activation of ERK1/2 induced by recombinant proteins of AREG and EREG were not inhibited by gefitinib. (F) Schematic diagram of the proposed mechanism by which AREG and EREG promote hepatocyte proliferation and partial epithelial–mesenchymal transition. (G) Immunofluorescence analysis revealed higher expression of EGFR in hepatocytes of rat tissues in zone 1 and zone 2 than in zone 3. (H) Schematic diagram of the application scheme of gefitinib and vehicle. (I) The future liver weight (FLW) to body weight (BW) ratio was calculated after PVL 48 h in the vehicle and gefitinib groups. (J, K) Immunofluorescence staining of Ki67 and PCNA in liver sections from DMSO ( n = 3) and gefitinib ( n = 3) rats at 48 h after PVL. Ki67-and PCNA-positive hepatocytes were counted in three PV-CV fields, and the average count of these three fields was set as the Ki67-and PCNA-positive cell number of one rat. (L) Gefitinib inhibited the proliferation of S5–S7 hepatocytes at 48 h after PVL and delayed liver regeneration. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests.

Journal: Genes & Diseases

Article Title: EGFR-mediated crosstalk between vascular endothelial cells and hepatocytes promotes Piezo1-dependent liver regeneration

doi: 10.1016/j.gendis.2024.101321

Figure Lengend Snippet: EGFR mediates hepatocyte proliferation and liver regeneration. (A) WB revealed that EGFR was activated by recombinant proteins of AREG (50 ng/mL) and EREG (20 ng/mL) in LO2 cells. (B) The MTT assay at 24 and 48 h suggested that gefitinib could block the proliferation of hepatocytes induced by AREG (50 ng/mL) and EREG (20 ng/mL) in LO2 cells (the results of statistical analysis were obtained by comparing with the 0 μM Gef group, respectively). (C) WB demonstrated that ERK1/2 was activated by recombinant proteins of AREG (50 ng/mL) and EREG (20 ng/mL) in LO2 cells. (D) The MTT assay confirmed that the proliferation of LO2 cells induced by AREG and EREG was partially reversed by ravoxertinib (ERK1/2 inhibitor) (the results of statistical analysis were obtained by comparing with the AREG+DMSO group). (E) WB indicated that activation of ERK1/2 induced by recombinant proteins of AREG and EREG were not inhibited by gefitinib. (F) Schematic diagram of the proposed mechanism by which AREG and EREG promote hepatocyte proliferation and partial epithelial–mesenchymal transition. (G) Immunofluorescence analysis revealed higher expression of EGFR in hepatocytes of rat tissues in zone 1 and zone 2 than in zone 3. (H) Schematic diagram of the application scheme of gefitinib and vehicle. (I) The future liver weight (FLW) to body weight (BW) ratio was calculated after PVL 48 h in the vehicle and gefitinib groups. (J, K) Immunofluorescence staining of Ki67 and PCNA in liver sections from DMSO ( n = 3) and gefitinib ( n = 3) rats at 48 h after PVL. Ki67-and PCNA-positive hepatocytes were counted in three PV-CV fields, and the average count of these three fields was set as the Ki67-and PCNA-positive cell number of one rat. (L) Gefitinib inhibited the proliferation of S5–S7 hepatocytes at 48 h after PVL and delayed liver regeneration. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests.

Article Snippet: Levels of AREG and EREG were measured using AREG (EK0304) and EREG (EK1394) ELISA kits from Boster Biological Technology (Wuhan, China) following the manufacturer's protocol.

Techniques: Recombinant, MTT Assay, Blocking Assay, Activation Assay, Immunofluorescence, Expressing, Staining, Two Tailed Test

Yoda1 improves fasting-induced poor liver regeneration in vivo . (A) Ultrasound was used to evaluate the portal vein blood flow velocity in the control and the fasting group (18 h after PVL, n = 2). (B) Fasting induced a decrease in the velocity of portal vein blood flow in rats. (C, D) Ki67 staining was used to evaluate liver regeneration in the control and fasting group at 24 h after PVL ( n = 3). (E, F) Under fasting conditions, Yoda1 promoted the expression of Ki67 in the regenerated liver (six different PV-CV ranges were selected for each rat right liver section to calculate the number of Ki67 positive cells. Vehicle group: n = 3; Yoda1 group: n = 4; Yoda1: 1 mg/kg). (G) Schematic of the mechanism by which piezo1 activation mediates endothelial and hepatocyte crosstalk during liver regeneration. After PVE, PVL, partial hepatectomy (PH), and ALPPS, the change of portal vein blood flow causes the imbalance of intrahepatic mechanical homeostasis. The activation of Piezo1 in endothelial cells can promote the expression of HBEGF, EREG, and AREG, and then activate the EGFR of hepatocytes, thus promoting the proliferation of hepatocytes and EMT. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests. ALPPS, associated liver partition and portal vein ligation for staged hepatectomy.

Journal: Genes & Diseases

Article Title: EGFR-mediated crosstalk between vascular endothelial cells and hepatocytes promotes Piezo1-dependent liver regeneration

doi: 10.1016/j.gendis.2024.101321

Figure Lengend Snippet: Yoda1 improves fasting-induced poor liver regeneration in vivo . (A) Ultrasound was used to evaluate the portal vein blood flow velocity in the control and the fasting group (18 h after PVL, n = 2). (B) Fasting induced a decrease in the velocity of portal vein blood flow in rats. (C, D) Ki67 staining was used to evaluate liver regeneration in the control and fasting group at 24 h after PVL ( n = 3). (E, F) Under fasting conditions, Yoda1 promoted the expression of Ki67 in the regenerated liver (six different PV-CV ranges were selected for each rat right liver section to calculate the number of Ki67 positive cells. Vehicle group: n = 3; Yoda1 group: n = 4; Yoda1: 1 mg/kg). (G) Schematic of the mechanism by which piezo1 activation mediates endothelial and hepatocyte crosstalk during liver regeneration. After PVE, PVL, partial hepatectomy (PH), and ALPPS, the change of portal vein blood flow causes the imbalance of intrahepatic mechanical homeostasis. The activation of Piezo1 in endothelial cells can promote the expression of HBEGF, EREG, and AREG, and then activate the EGFR of hepatocytes, thus promoting the proliferation of hepatocytes and EMT. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; two-tailed Student's t -tests. ALPPS, associated liver partition and portal vein ligation for staged hepatectomy.

Article Snippet: Levels of AREG and EREG were measured using AREG (EK0304) and EREG (EK1394) ELISA kits from Boster Biological Technology (Wuhan, China) following the manufacturer's protocol.

Techniques: In Vivo, Control, Staining, Expressing, Activation Assay, Two Tailed Test, Ligation

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