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recombinant 452 human epidermal growth factor  (R&D Systems)


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    Structured Review

    R&D Systems recombinant 452 human epidermal growth factor
    Recombinant 452 Human Epidermal Growth Factor, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 152 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+hb+egf+protein/Recombinant+Human+HB-EGF+Protein%2C+CF/10__1016_slash_j__isci__2026__115584-201-68-75
    Average 95 stars, based on 152 article reviews
    recombinant 452 human epidermal growth factor - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Migration:

    Article Title: Heparin-binding epidermal growth factor contributes to COPD disease severity by modulating airway fibrosis and pulmonary epithelial-mesenchymal transition.
    Article Snippet: Western blot analysis was used to detect changes in collagen types I and III, α-smooth muscle actin (SMA), mitogenactivated protein kinase (ERK/MAPK), phosphorylated ERK (p-ERK), p38, phosphorylated (p-p38) (Cell Signaling Technology, USA), N-cadherin and E-cadherin (Proteinthech, Chicago, USA), and vimentin (D21H3) (CST, Beverly, MA, USA) as previously described [11]. .. Cell viability assays, migration and proliferation To investigate HB-EGF’s effects on tissue fibrosis, human lung fibroblasts were treated with different doses of recombinant human HB-EGF protein (R&D Systems, Minneapolis, USA) for 48 h. Cells were seeded into a 96- well plate at a density of 1 × 104 cells/well. .. The cells were assayed with a cell counting kit (CCK)-8 (Liankebio, Hangzhou, China), which was used in order to determine cell proliferation according to the manufacturer’s instructions.

    Recombinant:

    Article Title: Heparin-binding epidermal growth factor contributes to COPD disease severity by modulating airway fibrosis and pulmonary epithelial-mesenchymal transition.
    Article Snippet: Western blot analysis was used to detect changes in collagen types I and III, α-smooth muscle actin (SMA), mitogenactivated protein kinase (ERK/MAPK), phosphorylated ERK (p-ERK), p38, phosphorylated (p-p38) (Cell Signaling Technology, USA), N-cadherin and E-cadherin (Proteinthech, Chicago, USA), and vimentin (D21H3) (CST, Beverly, MA, USA) as previously described [11]. .. Cell viability assays, migration and proliferation To investigate HB-EGF’s effects on tissue fibrosis, human lung fibroblasts were treated with different doses of recombinant human HB-EGF protein (R&D Systems, Minneapolis, USA) for 48 h. Cells were seeded into a 96- well plate at a density of 1 × 104 cells/well. .. The cells were assayed with a cell counting kit (CCK)-8 (Liankebio, Hangzhou, China), which was used in order to determine cell proliferation according to the manufacturer’s instructions.

    Article Title: HB-EGF induces mitochondrial dysfunction via estrogen hypersecretion in granulosa cells dependent on cAMP-PKA-JNK/ERK-Ca 2+ -FOXO1 pathway
    Article Snippet: .. Human KGN ovarian GCs (Biobw) were incubated with recombinant human HB-EGF protein (rHB-EGF, 20 ng/ml, R&D Systems) for 12 h in the absence or presence of EGFR inhibitor PF299804 (500 nM, Selleck), protein kinase A (PKA) inhibitor H89 (10 μM, Selleck), c-Jun N-terminal kinase (JNK) inhibitor SP600125 (20 mM, Selleck), extracellular signal-regulated kinase (ERK) inhibitor GDC-0994 (10 μM, Selleck), intracellular calcium ion (Ca 2+ ) chelator BAPTA-AM (20 μM, Selleck), forkhead box O 1 (FOXO1) inhibitor AS1842856 (10 μM, MCE), estrogen receptor antagonist ICI 182780 (0.1 μΜ, MCE) and mitochondrial permeability transition pore (mPTP) opening inhibitor ER-000444793 (2 μM, MCE). .. In addition, after treatment with rHB-EGF and EGFR inhibitor PF299804, cells were supplemented with cAMP analogue 8-bromoadenosine-cAMP (8-Br-cAMP, 500 μM, Sigma).

    Article Title: HB-EGF Ameliorates Oxidative Stress-Mediated Uterine Decidualization Damage
    Article Snippet: Uterine stromal cells from day 4 of pregnancy were isolated by enzymatic digestion as previously described [ ] and induced for in vitro decidualization with fresh medium supplemented with estradiol-17 β (Sigma, E1024, 10 nM) and progesterone (Sigma, 850454, 1 μ M) in DMEM-F12 with 2% charcoal-treated FBS (Gibco, 12676-029). .. After treatment with recombinant human HB-EGF protein (rHB-EGF, R&D Systems, 259-HE, 100 ng/ml), stromal cells were subjected to in vitro decidualization. .. For further studies, stromal cells were treated as described above and then exposed to 100 μ M H 2 O 2 for 4 h in the absence or presence of ROS scavenger N-acetyl-L-cysteine (NAC, Beyotime, S0017, 5 mM), GPX inhibitor Mercaptosuccinic Acid (MS, Sigma, V900745, 300 μ M), mitochondrial respiratory chain complex I inhibitor Rotenone (ROT, MCE, HY-B1756, 2 μ M), and mitochondrial respiratory chain complex III inhibitor Antimycin A (AA, Abcam, ab141904, 2 μ M).

    Article Title: HB-EGF Ameliorates Oxidative Stress-Mediated Uterine Decidualization Damage.
    Article Snippet: Isolation and Treatment of Uterine Stromal Cells.Uterine stromal cells from day 4 of pregnancy were isolated by enzymatic digestion as previously described [13] and induced for in vitro decidualization with fresh medium supplemented with estradiol-17β (Sigma, E1024, 10 nM) and progesterone (Sigma, 850454, 1μM) in DMEM-F12 with 2% charcoaltreated FBS (Gibco, 12676-029). .. After treatment with recombinant human HB-EGF protein (rHB-EGF, R&D Systems, 259-HE, 100 ng/ml), stromal cells were subjected to in vitro decidualization. .. For further studies, stromal cells were treated as described above and then exposed to 100μM H2O2 for 4 h in the absence or presence of ROS scavenger N-acetyl-L-cysteine (NAC, Beyotime, S0017, 5mM), GPX inhibitor Mercaptosuccinic Acid (MS, Sigma, V900745, 300μM), mitochondrial respiratory chain complex I inhibitor Rotenone (ROT, MCE, HY-B1756, 2μM), and mitochondrial respiratory chain complex III inhibitor Antimycin A (AA, Abcam, ab141904, 2μM).

    Incubation:

    Article Title: HB-EGF induces mitochondrial dysfunction via estrogen hypersecretion in granulosa cells dependent on cAMP-PKA-JNK/ERK-Ca 2+ -FOXO1 pathway
    Article Snippet: .. Human KGN ovarian GCs (Biobw) were incubated with recombinant human HB-EGF protein (rHB-EGF, 20 ng/ml, R&D Systems) for 12 h in the absence or presence of EGFR inhibitor PF299804 (500 nM, Selleck), protein kinase A (PKA) inhibitor H89 (10 μM, Selleck), c-Jun N-terminal kinase (JNK) inhibitor SP600125 (20 mM, Selleck), extracellular signal-regulated kinase (ERK) inhibitor GDC-0994 (10 μM, Selleck), intracellular calcium ion (Ca 2+ ) chelator BAPTA-AM (20 μM, Selleck), forkhead box O 1 (FOXO1) inhibitor AS1842856 (10 μM, MCE), estrogen receptor antagonist ICI 182780 (0.1 μΜ, MCE) and mitochondrial permeability transition pore (mPTP) opening inhibitor ER-000444793 (2 μM, MCE). .. In addition, after treatment with rHB-EGF and EGFR inhibitor PF299804, cells were supplemented with cAMP analogue 8-bromoadenosine-cAMP (8-Br-cAMP, 500 μM, Sigma).

    Permeability:

    Article Title: HB-EGF induces mitochondrial dysfunction via estrogen hypersecretion in granulosa cells dependent on cAMP-PKA-JNK/ERK-Ca 2+ -FOXO1 pathway
    Article Snippet: .. Human KGN ovarian GCs (Biobw) were incubated with recombinant human HB-EGF protein (rHB-EGF, 20 ng/ml, R&D Systems) for 12 h in the absence or presence of EGFR inhibitor PF299804 (500 nM, Selleck), protein kinase A (PKA) inhibitor H89 (10 μM, Selleck), c-Jun N-terminal kinase (JNK) inhibitor SP600125 (20 mM, Selleck), extracellular signal-regulated kinase (ERK) inhibitor GDC-0994 (10 μM, Selleck), intracellular calcium ion (Ca 2+ ) chelator BAPTA-AM (20 μM, Selleck), forkhead box O 1 (FOXO1) inhibitor AS1842856 (10 μM, MCE), estrogen receptor antagonist ICI 182780 (0.1 μΜ, MCE) and mitochondrial permeability transition pore (mPTP) opening inhibitor ER-000444793 (2 μM, MCE). .. In addition, after treatment with rHB-EGF and EGFR inhibitor PF299804, cells were supplemented with cAMP analogue 8-bromoadenosine-cAMP (8-Br-cAMP, 500 μM, Sigma).

    In Vitro:

    Article Title: HB-EGF Ameliorates Oxidative Stress-Mediated Uterine Decidualization Damage
    Article Snippet: Uterine stromal cells from day 4 of pregnancy were isolated by enzymatic digestion as previously described [ ] and induced for in vitro decidualization with fresh medium supplemented with estradiol-17 β (Sigma, E1024, 10 nM) and progesterone (Sigma, 850454, 1 μ M) in DMEM-F12 with 2% charcoal-treated FBS (Gibco, 12676-029). .. After treatment with recombinant human HB-EGF protein (rHB-EGF, R&D Systems, 259-HE, 100 ng/ml), stromal cells were subjected to in vitro decidualization. .. For further studies, stromal cells were treated as described above and then exposed to 100 μ M H 2 O 2 for 4 h in the absence or presence of ROS scavenger N-acetyl-L-cysteine (NAC, Beyotime, S0017, 5 mM), GPX inhibitor Mercaptosuccinic Acid (MS, Sigma, V900745, 300 μ M), mitochondrial respiratory chain complex I inhibitor Rotenone (ROT, MCE, HY-B1756, 2 μ M), and mitochondrial respiratory chain complex III inhibitor Antimycin A (AA, Abcam, ab141904, 2 μ M).

    Article Title: HB-EGF Ameliorates Oxidative Stress-Mediated Uterine Decidualization Damage.
    Article Snippet: Isolation and Treatment of Uterine Stromal Cells.Uterine stromal cells from day 4 of pregnancy were isolated by enzymatic digestion as previously described [13] and induced for in vitro decidualization with fresh medium supplemented with estradiol-17β (Sigma, E1024, 10 nM) and progesterone (Sigma, 850454, 1μM) in DMEM-F12 with 2% charcoaltreated FBS (Gibco, 12676-029). .. After treatment with recombinant human HB-EGF protein (rHB-EGF, R&D Systems, 259-HE, 100 ng/ml), stromal cells were subjected to in vitro decidualization. .. For further studies, stromal cells were treated as described above and then exposed to 100μM H2O2 for 4 h in the absence or presence of ROS scavenger N-acetyl-L-cysteine (NAC, Beyotime, S0017, 5mM), GPX inhibitor Mercaptosuccinic Acid (MS, Sigma, V900745, 300μM), mitochondrial respiratory chain complex I inhibitor Rotenone (ROT, MCE, HY-B1756, 2μM), and mitochondrial respiratory chain complex III inhibitor Antimycin A (AA, Abcam, ab141904, 2μM).



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