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ProSpec recombinant mouse hb-egf protein
Recombinant Mouse Hb Egf Protein, supplied by ProSpec, 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

recombinant mouse hb-egf protein - by Bioz Stars, 2026-09

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Article Title: Exogenous administration of heparin-binding epidermal growth factor-like growth factor improves erectile function in mice with bilateral cavernous nerve injury.
Article Snippet: The mice were divided into five groups (n = 9 for each group) as follows: sham operation group (in which the prostate and cavernous nerves were exposed during surgery but without direct physical intervention), and mice with bilateral CNI receiving two successive intracavernous injections (the first injection was given immediately after the model was made, and the second injection was given 3 days after the first injection) of phosphate-buffered saline (PBS; 20 μl), or three different doses (1 μg, 5 μg, and 10 μg) of recombinant mouse HB-EGF protein (ProSpec, East Brunswick, NJ, USA).

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Host HB-EGF inhibits ASFV infection by blocking viral attachment and internalization in vitro. A PAMs were infected with purified ASFV-WT (MOI = 2) at 37 °C for 0, 6, 12, and 24 h, respectively. The HB-EGF mRNA expression levels were detected by qPCR. MA-104 cells were transfected with HB-EGF for 24 h, followed by infection with ASFV-WT (MOI = 0.1) at 37 °C for 24 h. The ASFV infection was detected by western blot ( B ) and qPCR ( C ). HB-EGF stable expression MA-104 cells were infected with ASFV-WT (MOI = 0.1) at 37 °C for 24 h. The ASFV infection was detected by western blot ( D ) and qPCR ( E ). HB-EGF-KD MA-104 cells were infected with ASFV-WT (MOI = 0.1) at 37 °C for 24 h. The ASFV infection was detected by western blot ( F ) and qPCR ( G ). The attachment ( H ) and internalization ( I ) of ASFV in Wild-type, HB-EGF stable expression, and HB-EGF-KD MA-104 cells were detected by qPCR. The attachment ( J ) and internalization ( K ) of DiD-ASFV were observed by ZEISS LSM980. The cell membrane stained with green markers was used as a reference, where the cell membrane was colocalized (red) with the binding virus. The attachment ( L ) and internalization ( M ) were counted. More than 100 cells were counted per sample, and the number of cells that bound DiD-ASFV was calculated

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Heparan sulfate as an attachment factor for ASFV is restricted by host HB-EGF

doi: 10.1007/s00018-026-06188-z

Figure Lengend Snippet: Host HB-EGF inhibits ASFV infection by blocking viral attachment and internalization in vitro. A PAMs were infected with purified ASFV-WT (MOI = 2) at 37 °C for 0, 6, 12, and 24 h, respectively. The HB-EGF mRNA expression levels were detected by qPCR. MA-104 cells were transfected with HB-EGF for 24 h, followed by infection with ASFV-WT (MOI = 0.1) at 37 °C for 24 h. The ASFV infection was detected by western blot ( B ) and qPCR ( C ). HB-EGF stable expression MA-104 cells were infected with ASFV-WT (MOI = 0.1) at 37 °C for 24 h. The ASFV infection was detected by western blot ( D ) and qPCR ( E ). HB-EGF-KD MA-104 cells were infected with ASFV-WT (MOI = 0.1) at 37 °C for 24 h. The ASFV infection was detected by western blot ( F ) and qPCR ( G ). The attachment ( H ) and internalization ( I ) of ASFV in Wild-type, HB-EGF stable expression, and HB-EGF-KD MA-104 cells were detected by qPCR. The attachment ( J ) and internalization ( K ) of DiD-ASFV were observed by ZEISS LSM980. The cell membrane stained with green markers was used as a reference, where the cell membrane was colocalized (red) with the binding virus. The attachment ( L ) and internalization ( M ) were counted. More than 100 cells were counted per sample, and the number of cells that bound DiD-ASFV was calculated

Article Snippet: Surfen dihydrochloride, mitoxantrone, heparin, heparan sulfate, DiD perchlorate, and recombinant HB-EGF eukaryotic expression protein were purchased from MedChemExpress (USA).

Techniques: Infection, Blocking Assay, In Vitro, Purification, Expressing, Transfection, Western Blot, Membrane, Staining, Binding Assay, Virus

HB-EGF inhibits ASFV infection by the Heparin Binding domain. Schematic diagram of HB-EGF domain structure ( A ) and the truncation mutants ( B ) used to determine the antiviral domain. MA-104 cells were transfected with HB-EGF-Full, HB-EGF-ΔED, and HB-EGF-ΔHBD, followed by infection with ASFV-WT (MOI = 0.1) at 37 °C for 24 h. The ASFV infection was detected by western blot ( C ) and qPCR ( D ). Schematic diagram of HBD-derived peptide sequence ( E ). The affinity of the peptide for heparin ( F ) and heparan sulfate ( G ) was detected by Bio-Layer Interferometry. PAMs were pretreated with different concentrations of peptide, followed by infection with ASFV-WT (MOI = 0.1) at 37 °C for 24 h ( H ). ASFV p72 protein and mRNA expression were assessed by western blot ( I ) and qPCR ( J ). The progeny virus production was quantified by the HDA50 assay ( K ). Recombinant HB-EGF (200 ng/ml) was used to pretreat PAMs at 37 °C for 6 h in the presence or absence of Heparin (200 ng/ml), followed by infection with ASFV-WT/GFP (MOI = 0.1) at 37 °C for the indicated time points ( L ). ASFV infection was quantified by western blot ( M ), fluorescence microscopy ( N , O ), and HAD50 assay ( P )

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Heparan sulfate as an attachment factor for ASFV is restricted by host HB-EGF

doi: 10.1007/s00018-026-06188-z

Figure Lengend Snippet: HB-EGF inhibits ASFV infection by the Heparin Binding domain. Schematic diagram of HB-EGF domain structure ( A ) and the truncation mutants ( B ) used to determine the antiviral domain. MA-104 cells were transfected with HB-EGF-Full, HB-EGF-ΔED, and HB-EGF-ΔHBD, followed by infection with ASFV-WT (MOI = 0.1) at 37 °C for 24 h. The ASFV infection was detected by western blot ( C ) and qPCR ( D ). Schematic diagram of HBD-derived peptide sequence ( E ). The affinity of the peptide for heparin ( F ) and heparan sulfate ( G ) was detected by Bio-Layer Interferometry. PAMs were pretreated with different concentrations of peptide, followed by infection with ASFV-WT (MOI = 0.1) at 37 °C for 24 h ( H ). ASFV p72 protein and mRNA expression were assessed by western blot ( I ) and qPCR ( J ). The progeny virus production was quantified by the HDA50 assay ( K ). Recombinant HB-EGF (200 ng/ml) was used to pretreat PAMs at 37 °C for 6 h in the presence or absence of Heparin (200 ng/ml), followed by infection with ASFV-WT/GFP (MOI = 0.1) at 37 °C for the indicated time points ( L ). ASFV infection was quantified by western blot ( M ), fluorescence microscopy ( N , O ), and HAD50 assay ( P )

Article Snippet: Surfen dihydrochloride, mitoxantrone, heparin, heparan sulfate, DiD perchlorate, and recombinant HB-EGF eukaryotic expression protein were purchased from MedChemExpress (USA).

Techniques: Infection, Binding Assay, Transfection, Western Blot, Derivative Assay, Sequencing, Expressing, Virus, Recombinant, Fluorescence, Microscopy

Fig. 3 The EGFR-JNK2 axis is involved in sorafenib-induced hyper-keratosis. a HaCaT cells were transfected with non-targeting siRNA or siRNA targeting EGFR. The transcription level of EGFR was detected by RT-qPCR (upper panel, n = 3) and the expression level of EGFR was determined by western blot (lower panel). b–e HaCaT cells were transfected with non-targeting siRNA or siRNA targeting EGFR, followed by treatment with CdMCTRL or CdMSORA for 24 h (b, d) or treatment with or without s-HBEGF (2.5 ng/mL) for 24 h (c, e). The cell survival rates were measured by SRB assay (n = 3) (b, c). The transcription levels of KRT1, KRT10, LORICRIN and IVL were measured by RT-qPCR (n = 3) (d, e). f Relevant EGFR downstream signaling pathways were examined by western blot. g Human primary keratinocytes were treated with s-HBEGF and the expression levels of p-JNK1/2, JNK2, p-JNK1 and JNK1 were assessed by western blot. h HaCaT cells or human primary keratinocytes were treated with or without sorafenib, CdMCTRL or CdMSORA. The expression levels of p-JNK1/2, JNK2, p-JNK1 and JNK1 were assessed by western blot. i HaCaT cells were transfected with non-targeting siRNA or siRNA targeting JNK2. JNK2 transcription level was detected by RT- qPCR (upper panel, n = 3) and the expression level of JNK2 was determined by western blot (lower panel). j–m HaCaT cells were transfected with non-targeting siRNA or siRNA targeting JNK2, followed by treatment with CdMCTRL or CdMSORA for 24 h (j, l) or treatment with or without s-HBEGF (2.5 ng/mL) for 24 h (k, m). The transcription levels of KRT1, KRT10, LORICRIN and IVL were measured by RT-qPCR (n = 3) (j, k). The cell survival rates were measured by SRB assay (n = 3) (l, m). Densitometric values are shown as optical density after ACTB or GAPDH normalization using Image J. The results in (a), (b), (c), (d), (e), (i), (j), (k), (l) and (m) are presented as the mean ± SD. Statistical analyses were performed using one-way ANOVA with Dunn’s post hoc test in (a), (i) and when comparing the levels of KRT1 in (j) and with LSD post hoc test in (d), (e), (k) and when comparing the levels of KRT10, LORICRIN and IVL in (j). n.s. no signiﬁcance; *P < 0.05; **P < 0.01; ***P < 0.001. SORA sorafenib, CdM HUVECs conditional medium, CTRL control.

Journal: Cell research

Article Title: s-HBEGF/SIRT1 circuit-dictated crosstalk between vascular endothelial cells and keratinocytes mediates sorafenib-induced hand-foot skin reaction that can be reversed by nicotinamide.

doi: 10.1038/s41422-020-0309-6

Figure Lengend Snippet: Fig. 3 The EGFR-JNK2 axis is involved in sorafenib-induced hyper-keratosis. a HaCaT cells were transfected with non-targeting siRNA or siRNA targeting EGFR. The transcription level of EGFR was detected by RT-qPCR (upper panel, n = 3) and the expression level of EGFR was determined by western blot (lower panel). b–e HaCaT cells were transfected with non-targeting siRNA or siRNA targeting EGFR, followed by treatment with CdMCTRL or CdMSORA for 24 h (b, d) or treatment with or without s-HBEGF (2.5 ng/mL) for 24 h (c, e). The cell survival rates were measured by SRB assay (n = 3) (b, c). The transcription levels of KRT1, KRT10, LORICRIN and IVL were measured by RT-qPCR (n = 3) (d, e). f Relevant EGFR downstream signaling pathways were examined by western blot. g Human primary keratinocytes were treated with s-HBEGF and the expression levels of p-JNK1/2, JNK2, p-JNK1 and JNK1 were assessed by western blot. h HaCaT cells or human primary keratinocytes were treated with or without sorafenib, CdMCTRL or CdMSORA. The expression levels of p-JNK1/2, JNK2, p-JNK1 and JNK1 were assessed by western blot. i HaCaT cells were transfected with non-targeting siRNA or siRNA targeting JNK2. JNK2 transcription level was detected by RT- qPCR (upper panel, n = 3) and the expression level of JNK2 was determined by western blot (lower panel). j–m HaCaT cells were transfected with non-targeting siRNA or siRNA targeting JNK2, followed by treatment with CdMCTRL or CdMSORA for 24 h (j, l) or treatment with or without s-HBEGF (2.5 ng/mL) for 24 h (k, m). The transcription levels of KRT1, KRT10, LORICRIN and IVL were measured by RT-qPCR (n = 3) (j, k). The cell survival rates were measured by SRB assay (n = 3) (l, m). Densitometric values are shown as optical density after ACTB or GAPDH normalization using Image J. The results in (a), (b), (c), (d), (e), (i), (j), (k), (l) and (m) are presented as the mean ± SD. Statistical analyses were performed using one-way ANOVA with Dunn’s post hoc test in (a), (i) and when comparing the levels of KRT1 in (j) and with LSD post hoc test in (d), (e), (k) and when comparing the levels of KRT10, LORICRIN and IVL in (j). n.s. no signiﬁcance; *P < 0.05; **P < 0.01; ***P < 0.001. SORA sorafenib, CdM HUVECs conditional medium, CTRL control.

Article Snippet: Mouse HBEGF recombinant protein (Novus Biologicals, NBP235069-10 ug) was used in vivo (25 ng per mouse).

Techniques: Transfection, Quantitative RT-PCR, Expressing, Western Blot, Sulforhodamine B Assay, Protein-Protein interactions, Control

Fig. 4 s-HBEGF stabilizes SIRT1 in keratinocytes by increasing its phosphorylation at Ser 27 via JNK2. a HaCaT cells or human primary keratinocytes were treated with or without sorafenib, CdMCTRL or CdMSORA. The expression level of SIRT1 was detected by western blot. b HaCaT cells or human primary keratinocytes were treated with s-HBEGF for 24 h. The expression level of SIRT1 was analyzed by western blot. c Representative western blot indicated the expression of SIRT1 in the stratum corneum of mice in control or sorafenib-treated group (n = 5/ group). d Representative western blot indicated the expression of SIRT1 in the stratum corneum of mice in control or s-HBEGF-treated group (n = 5/group). e Representative immunohistochemistry images showing SIRT1-stained paws of mice in control, sorafenib, HBEGF neutralizing antibody or combination group (left panel). Representative immunohistochemistry images showing SIRT1-stained paws of mice with or without s-HBEGF treatment (right panel). Scale bar, 50 µm. f HaCaT cells were transfected with non-targeting siRNA or siRNA targeting JNK2, followed by treatment with or without s-HBEGF (2.5 ng/mL) for 24 h. The expression levels of p-JNK1/2, JNK2 and SIRT1 were determined by western blot. g HaCaT cells were treated with s-HBEGF for 24 h. The transcription level of SIRT1 was measured by RT-qPCR (n = 3). h HaCaT cells were treated with CHX with or without s-HBEGF at different time points, and SIRT1 protein level was measured by western blot. i HaCaT cells were treated with s-HBEGF for 24 h. The expression levels of p-SIRT1 and SIRT1 were analyzed by western blot. j Human primary keratinocytes were treated with s-HBEGF for 24 h. The expression levels of p-SIRT1 and SIRT1 were analyzed by western blot. k HaCaT cells were treated with s-HBEGF for 24 h. Cell lysates were immunoprecipitated with anti-SIRT1 antibody and probed with anti-Ub antibody or with anti-SIRT1 antibody. Protein expression levels of endogenous p-SIRT1 and SIRT1 are displayed. l HaCaT cells were transfected with non-targeting siRNA or siRNA targeting JNK2, followed by treatment with or without s-HBEGF (2.5 ng/mL) for 24 h. Cell lysates were immunoprecipitated with anti- SIRT1 antibody and probed with anti-Ub antibody or with anti-SIRT1 antibody. Protein expression levels of endogenous p-SIRT1, SIRT1, p- JNK1/2, JNK2 are displayed. Densitometric values are shown as optical density after ACTB or GAPDH normalization using Image J. The results in (g) are presented as the mean ± SD. Statistical analyses were performed using one-way ANOVA with LSD post hoc test in (g). n.s. no signiﬁcance. SORA sorafenib, CHX cycloheximide, CdM HUVECs conditional medium, CTRL control, IP immunoprecipitant, WCL whole cell lysate.

Journal: Cell research

doi: 10.1038/s41422-020-0309-6

Figure Lengend Snippet: Fig. 4 s-HBEGF stabilizes SIRT1 in keratinocytes by increasing its phosphorylation at Ser 27 via JNK2. a HaCaT cells or human primary keratinocytes were treated with or without sorafenib, CdMCTRL or CdMSORA. The expression level of SIRT1 was detected by western blot. b HaCaT cells or human primary keratinocytes were treated with s-HBEGF for 24 h. The expression level of SIRT1 was analyzed by western blot. c Representative western blot indicated the expression of SIRT1 in the stratum corneum of mice in control or sorafenib-treated group (n = 5/ group). d Representative western blot indicated the expression of SIRT1 in the stratum corneum of mice in control or s-HBEGF-treated group (n = 5/group). e Representative immunohistochemistry images showing SIRT1-stained paws of mice in control, sorafenib, HBEGF neutralizing antibody or combination group (left panel). Representative immunohistochemistry images showing SIRT1-stained paws of mice with or without s-HBEGF treatment (right panel). Scale bar, 50 µm. f HaCaT cells were transfected with non-targeting siRNA or siRNA targeting JNK2, followed by treatment with or without s-HBEGF (2.5 ng/mL) for 24 h. The expression levels of p-JNK1/2, JNK2 and SIRT1 were determined by western blot. g HaCaT cells were treated with s-HBEGF for 24 h. The transcription level of SIRT1 was measured by RT-qPCR (n = 3). h HaCaT cells were treated with CHX with or without s-HBEGF at different time points, and SIRT1 protein level was measured by western blot. i HaCaT cells were treated with s-HBEGF for 24 h. The expression levels of p-SIRT1 and SIRT1 were analyzed by western blot. j Human primary keratinocytes were treated with s-HBEGF for 24 h. The expression levels of p-SIRT1 and SIRT1 were analyzed by western blot. k HaCaT cells were treated with s-HBEGF for 24 h. Cell lysates were immunoprecipitated with anti-SIRT1 antibody and probed with anti-Ub antibody or with anti-SIRT1 antibody. Protein expression levels of endogenous p-SIRT1 and SIRT1 are displayed. l HaCaT cells were transfected with non-targeting siRNA or siRNA targeting JNK2, followed by treatment with or without s-HBEGF (2.5 ng/mL) for 24 h. Cell lysates were immunoprecipitated with anti- SIRT1 antibody and probed with anti-Ub antibody or with anti-SIRT1 antibody. Protein expression levels of endogenous p-SIRT1, SIRT1, p- JNK1/2, JNK2 are displayed. Densitometric values are shown as optical density after ACTB or GAPDH normalization using Image J. The results in (g) are presented as the mean ± SD. Statistical analyses were performed using one-way ANOVA with LSD post hoc test in (g). n.s. no signiﬁcance. SORA sorafenib, CHX cycloheximide, CdM HUVECs conditional medium, CTRL control, IP immunoprecipitant, WCL whole cell lysate.

Article Snippet: Mouse HBEGF recombinant protein (Novus Biologicals, NBP235069-10 ug) was used in vivo (25 ng per mouse).

Techniques: Phospho-proteomics, Expressing, Western Blot, Control, Immunohistochemistry, Staining, Transfection, Quantitative RT-PCR, Immunoprecipitation

Fig. 6 Classic SIRT1 inhibitor nicotinamide could relieve sorafenib-induced HFSR. a HaCaT cells were treated with or without 10 mM nicotinamide, followed by treatment with CdMCTRL or CdMSORA for 24 h. The transcription levels of KRT1, KRT10, LORICRIN and IVL were measured by RT-qPCR (n = 3). b–d Mice were treated with vehicle, sorafenib (100 mg/kg/day), nicotinamide (100 mg/kg/day) or sorafenib plus nicotinamide by intragastric administration for 30 days (n = 5/group). b Representative histopathology images show H&E-stained paws of the mice in control, sorafenib, nicotinamide or combination group. Representative immunohistochemistry images show KRT5, KRT1 or LORICRIN- stained paws of each group. Scale bar, 50 µm. c Thickness quantiﬁcation of corneous layer of paws of the mice in control, sorafenib, nicotinamide or combination group (n = 5/group). d s-HBEGF concentrations in the serum of each mouse were measured by ELISA (n = 5/ group). e Hands and feet of patients with sorafenib-induced HFSR showing hyper-keratosis before (left panel) and after (right panel) administration with 50 or 100 mg nicotinic acid (depending on HSFR grade) three times a day. f Diagnosis information of each patient. Horizontal bars in (c) and (d) represent mean values. The results in (a) are presented as the mean ± SD. Statistical analyses were performed using unpaired two-tailed Student’s t test in (a), and one-way ANOVA with LSD post hoc test in (c) and (d). n.s. no signiﬁcance; *P < 0.05; ***P < 0.001. NAM nicotinamide, SORA sorafenib, CdM HUVECs conditional medium, CTRL control.

Journal: Cell research

doi: 10.1038/s41422-020-0309-6

Figure Lengend Snippet: Fig. 6 Classic SIRT1 inhibitor nicotinamide could relieve sorafenib-induced HFSR. a HaCaT cells were treated with or without 10 mM nicotinamide, followed by treatment with CdMCTRL or CdMSORA for 24 h. The transcription levels of KRT1, KRT10, LORICRIN and IVL were measured by RT-qPCR (n = 3). b–d Mice were treated with vehicle, sorafenib (100 mg/kg/day), nicotinamide (100 mg/kg/day) or sorafenib plus nicotinamide by intragastric administration for 30 days (n = 5/group). b Representative histopathology images show H&E-stained paws of the mice in control, sorafenib, nicotinamide or combination group. Representative immunohistochemistry images show KRT5, KRT1 or LORICRIN- stained paws of each group. Scale bar, 50 µm. c Thickness quantiﬁcation of corneous layer of paws of the mice in control, sorafenib, nicotinamide or combination group (n = 5/group). d s-HBEGF concentrations in the serum of each mouse were measured by ELISA (n = 5/ group). e Hands and feet of patients with sorafenib-induced HFSR showing hyper-keratosis before (left panel) and after (right panel) administration with 50 or 100 mg nicotinic acid (depending on HSFR grade) three times a day. f Diagnosis information of each patient. Horizontal bars in (c) and (d) represent mean values. The results in (a) are presented as the mean ± SD. Statistical analyses were performed using unpaired two-tailed Student’s t test in (a), and one-way ANOVA with LSD post hoc test in (c) and (d). n.s. no signiﬁcance; *P < 0.05; ***P < 0.001. NAM nicotinamide, SORA sorafenib, CdM HUVECs conditional medium, CTRL control.

Article Snippet: Mouse HBEGF recombinant protein (Novus Biologicals, NBP235069-10 ug) was used in vivo (25 ng per mouse).

Techniques: Quantitative RT-PCR, Histopathology, Staining, Control, Immunohistochemistry, Enzyme-linked Immunosorbent Assay, Biomarker Discovery, Two Tailed Test

Fig. 7 Schematic representation of the mechanism underlying sorafenib-induced hyper-keratosis. Vascular endothelial cells release s-HBEGF upon sorafenib stimulation. s-HBEGF binds to EGFR and leads to JNK2 phosphorylation in keratinocytes. The activated JNK2 subsequently stabilizes SIRT1, which eventually results in keratinization. The classic SIRT1 inhibitor nicotinamide could effectively reverse sorafenib-induced HFSR.

Journal: Cell research

doi: 10.1038/s41422-020-0309-6

Figure Lengend Snippet: Fig. 7 Schematic representation of the mechanism underlying sorafenib-induced hyper-keratosis. Vascular endothelial cells release s-HBEGF upon sorafenib stimulation. s-HBEGF binds to EGFR and leads to JNK2 phosphorylation in keratinocytes. The activated JNK2 subsequently stabilizes SIRT1, which eventually results in keratinization. The classic SIRT1 inhibitor nicotinamide could effectively reverse sorafenib-induced HFSR.

Article Snippet: Mouse HBEGF recombinant protein (Novus Biologicals, NBP235069-10 ug) was used in vivo (25 ng per mouse).

Techniques: Phospho-proteomics

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