bdnf  (Alomone Labs)


Bioz Verified Symbol Alomone Labs is a verified supplier
Bioz Manufacturer Symbol Alomone Labs manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93
    Name:
    B 250 human BDNF
    Description:
    Human Brain Derived Neurotrophic Factor Recombinant E coli
    Catalog Number:
    B-250
    Price:
    242.0
    Category:
    Protein
    Source:
    Recombinant, E. coli
    Applications:
    0
    Purity:
    >98% (HPLC)
    Size:
    1 Vials containing 1 mcg each
    Format:
    Lyophilized from a 0.2 µm filtered solution.
    Molecular Weight:
    27 kDa.
    Molecule Name:
    BDNF, Brain-derived neurotrophic factor
    Buy from Supplier


    Structured Review

    Alomone Labs bdnf
    B 250 human BDNF
    Human Brain Derived Neurotrophic Factor Recombinant E coli
    https://www.bioz.com/result/bdnf/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bdnf - by Bioz Stars, 2021-09
    93/100 stars

    Images

    1) Product Images from "BDNF mediates non cell-autonomous regulation of sensory neuron position and identity"

    Article Title: BDNF mediates non cell-autonomous regulation of sensory neuron position and identity

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4025-10.2010

    Maintenance of DRG identity requires BDNF. A, Injection of NGF or (50 ng/mL) does not prevent the increase in migratory DRG neurons present in nav1.6 morphants (dashed grey line). In contrast, injection of BDNF or NT-3 reduces the number of migratory DRG neurons in nav1.6 morphants to levels found in wild type embryos (dashed black line). * and **, p
    Figure Legend Snippet: Maintenance of DRG identity requires BDNF. A, Injection of NGF or (50 ng/mL) does not prevent the increase in migratory DRG neurons present in nav1.6 morphants (dashed grey line). In contrast, injection of BDNF or NT-3 reduces the number of migratory DRG neurons in nav1.6 morphants to levels found in wild type embryos (dashed black line). * and **, p

    Techniques Used: Injection

    2) Product Images from "Astrocytes from cortex and striatum show differential responses to mitochondrial toxin and BDNF: implications for protection of striatal neurons expressing mutant huntingtin"

    Article Title: Astrocytes from cortex and striatum show differential responses to mitochondrial toxin and BDNF: implications for protection of striatal neurons expressing mutant huntingtin

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-020-01965-4

    BDNF modifies astrocyte cytokine release. Cortical and striatal astrocytes were treated for 24 h with 3NP 15 mM with or without BDNF 50 ng/ml ( a ) or with LPS 1 μg/ml with or without BDNF 50 ng/ml ( b ). TNF-α release into the culture supernatant was assessed by ELISA and normalized to viability values obtained with the MTT assay for each experimental group. Data are the mean ± SEM of n = 3 independent experiments. Differences between two groups were analyzed by Student’s t test. ^ p
    Figure Legend Snippet: BDNF modifies astrocyte cytokine release. Cortical and striatal astrocytes were treated for 24 h with 3NP 15 mM with or without BDNF 50 ng/ml ( a ) or with LPS 1 μg/ml with or without BDNF 50 ng/ml ( b ). TNF-α release into the culture supernatant was assessed by ELISA and normalized to viability values obtained with the MTT assay for each experimental group. Data are the mean ± SEM of n = 3 independent experiments. Differences between two groups were analyzed by Student’s t test. ^ p

    Techniques Used: Enzyme-linked Immunosorbent Assay, MTT Assay

    Related Articles

    other:

    Article Title: Sortilin gates neurotensin and BDNF signaling to control peripheral neuropathic pain
    Article Snippet: Human BDNF (7.5 μl) (1.5 μg per mouse; B-250, Alomone Labs) diluted in sterile PBS and sol-sortilin (8 μl; 10 μg per mouse) diluted in sterile PBS were prepared, as previously described ( ).

    Article Title: Novel metabolic role for BDNF in pancreatic β-cell insulin secretion
    Article Snippet: Brain-derived neurotrophic factor (BDNF) (B-250) was from Alomone labs.

    Recombinant:

    Article Title: Retrograde transport of Akt by a neuronal Rab5-APPL1 endosome
    Article Snippet: .. Neurons were plated on two wells on one side of the chamber and on the opposite side of the chamber recombinant human BDNF (Cat. n° B-250, Alomone Labs, Jerusalem, Israel) diluted in agarose was added. ..

    Article Title: STAT3-BDNF-TrkB signaling promotes alveolar epithelial regeneration after lung injury
    Article Snippet: .. After two days of culture, Y276632 was removed and ligand treatments of organoids were performed using the following reagents at the indicated concentrations: ANA-12 0.02μg/mL (Alomone Labs catalog #A-215), recombinant human BDNF 0.05μg/mL (Alomone Labs catalog #B-250) and recombinant murine FGF7 0.01μg/mL (R & D Systems catalog #5028-KG). ..

    Immunofluorescence:

    Article Title: Low-affinity neurotrophin receptor p75 of brain-derived neurotrophic factor contributes to cancer-induced bone pain by upregulating mTOR signaling
    Article Snippet: .. Immunofluorescence staining For the in vitro experiments, following 48 h of culture, DRG neurons were treated with exogenous BDNF (20 ng/ml; cat. no. B-250; Alomone Labs) for another 24 h, with the control group cultured in medium only (n=5 for each group). ..

    Staining:

    Article Title: Low-affinity neurotrophin receptor p75 of brain-derived neurotrophic factor contributes to cancer-induced bone pain by upregulating mTOR signaling
    Article Snippet: .. Immunofluorescence staining For the in vitro experiments, following 48 h of culture, DRG neurons were treated with exogenous BDNF (20 ng/ml; cat. no. B-250; Alomone Labs) for another 24 h, with the control group cultured in medium only (n=5 for each group). ..

    In Vitro:

    Article Title: Low-affinity neurotrophin receptor p75 of brain-derived neurotrophic factor contributes to cancer-induced bone pain by upregulating mTOR signaling
    Article Snippet: .. Immunofluorescence staining For the in vitro experiments, following 48 h of culture, DRG neurons were treated with exogenous BDNF (20 ng/ml; cat. no. B-250; Alomone Labs) for another 24 h, with the control group cultured in medium only (n=5 for each group). ..

    Cell Culture:

    Article Title: Low-affinity neurotrophin receptor p75 of brain-derived neurotrophic factor contributes to cancer-induced bone pain by upregulating mTOR signaling
    Article Snippet: .. Immunofluorescence staining For the in vitro experiments, following 48 h of culture, DRG neurons were treated with exogenous BDNF (20 ng/ml; cat. no. B-250; Alomone Labs) for another 24 h, with the control group cultured in medium only (n=5 for each group). ..

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93
    Alomone Labs recombinant human bdnf protein
    Rearing larvae in dim light reduces production of <t>BDNF</t> in the medial PGZ by 10 <t>dpf</t> ( A–C ). Scale bar, 15 μm. Injecting 5 dpf larvae with 100 ng/ml recombinant human BDNF increased the amount of BDNF protein detected by immunohistochemistry
    Recombinant Human Bdnf Protein, supplied by Alomone Labs, 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/recombinant human bdnf protein/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant human bdnf protein - by Bioz Stars, 2021-09
    93/100 stars
      Buy from Supplier

    92
    Alomone Labs biotin bdnf
    Pridopidine repairs axonal transport defects in SOD1 G93A MNs and further enhances axonal transport to a processive mode. a Schematic illustration of an experimental system for axonal transport tracking in MNs. Spinal cord (SC) explants from WT or SOD1 G93A E12.5 mouse embryos are plated in the proximal compartment of a microfluidic chamber. MNs from the spinal cord send their axons towards the distal compartment. At this point <t>Qdot-BDNF</t> is applied exclusively to this compartment. Axonal transport of Qdot-BDNF is then visualized and recorded by a high-resolution spinning disk confocal imaging system. b Time lapse images of Qdot-BDNF (bright orange) axonal transport as acquired at 60X magnification. Yellow arrowheads point to a single Qdot-BDNF particle that is retrogradely transported (left) towards the cell body. Scale bar: 10 µm. Bottom panel shows a kymograph of a complete Qdot-BDNF time-lapse movie. Scale bars: Horizontal 10 µm; vertical 100 s. c Bar chart of the Instantaneous Velocity values for Qdot-BDNF particles in WT (blue) or SOD1 G93A (red) MNs show slower velocities in the SOD1 G93A MNs. Pridopidine application accelerates the instantaneous velocities both in WT MNs (0.1 µM) and SOD1 G93A MNs (0.1 µM and 1 µM). Application of 25 µM or 100 µM Riluzole on SOD1 G93A MNs does not affect the instantaneous velocities. S1R − / − MNs reveal defects in the axonal transport of BDNF. Pridopidine at either 0.1 µM or 1 µM was unable to recover these defects (n = number of qDot-BDNF steps). d Bar chart of particle Stop-Count shows that pridopidine reduces the number of pauses during axonal transport in WT MNs (0.1 µM only) and SOD1 G93A MNs (both 0.1 µM and 1 µM). Axonal transport parameters of Qdot-BDNF in S1R − / − MNs show that unlike SOD G93A MNs, they are not responsive to pridopidine at any of the concentrations tested (n = number of Qdot-BDNF tracks). e , f Graphs showing the MSD over time for SOD1 G93A MNs e and S1R − / − MNs f show that pridopidine accelerates axonal transport in a S1R-dependent mechanism. g Distribution of average velocities of analyzed tracks in SOD1 G93A MNs shows a significant increase towards higher velocities in pridopidine-treated MNs. Dashed lines denote a polynomial fitting curve for each condition. Data are shown as the mean ± SEM. * p value
    Biotin Bdnf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/biotin bdnf/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    biotin bdnf - by Bioz Stars, 2021-09
    92/100 stars
      Buy from Supplier

    90
    Alomone Labs endothelin receptor b
    Effects of <t>endothelin-1</t> receptor blockade with tezosentan (TEZO) and nitric oxide synthase inhibition (L-NAME) on insulin-mediated vasorelaxtion of thoracic aortic rings of low-capacity running (LCR) and high-capacity running (HCR) rats. The left panels (A and B) present data from insulin dose-response curves in HCR, and right panel (C and D) present data from insulin dose-response curves in LCR. Closed circles represent % relaxation in response to insulin alone, open triangles represent % relaxation to insulin in the presence of 3 μ M TEZO a nonspecific inhibitor of ET-1 receptors (top panel, A and C) N = 9–16/group, and open squares represent % relaxation to insulin in the presence of 300 μ M L-NAME, a nitric oxide synthase inhibitor, (bottom panel, B and D) N = 6–8/group. Insulin μ IU/mL, micro-international units per milliliter. Values are expressed as means ± SEM. *Denotes line difference ( P
    Endothelin Receptor B, supplied by Alomone Labs, 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/result/endothelin receptor b/product/Alomone Labs
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    endothelin receptor b - by Bioz Stars, 2021-09
    90/100 stars
      Buy from Supplier

    Image Search Results


    Rearing larvae in dim light reduces production of BDNF in the medial PGZ by 10 dpf ( A–C ). Scale bar, 15 μm. Injecting 5 dpf larvae with 100 ng/ml recombinant human BDNF increased the amount of BDNF protein detected by immunohistochemistry

    Journal: The Journal of Neuroscience

    Article Title: Visual Experience Facilitates BDNF-Dependent Adaptive Recruitment of New Neurons in the Postembryonic Optic Tectum

    doi: 10.1523/JNEUROSCI.1962-17.2018

    Figure Lengend Snippet: Rearing larvae in dim light reduces production of BDNF in the medial PGZ by 10 dpf ( A–C ). Scale bar, 15 μm. Injecting 5 dpf larvae with 100 ng/ml recombinant human BDNF increased the amount of BDNF protein detected by immunohistochemistry

    Article Snippet: To test whether exogenous BDNF was detectable in whole-brain lysates following ICV injections, we performed a Western blot using 5 dpf larvae injected with either 100 ng/ml recombinant human BDNF protein (#B-250, Alomone Labs) or a vehicle control.

    Techniques: Recombinant, Immunohistochemistry

    Maintenance of DRG identity requires BDNF. A, Injection of NGF or (50 ng/mL) does not prevent the increase in migratory DRG neurons present in nav1.6 morphants (dashed grey line). In contrast, injection of BDNF or NT-3 reduces the number of migratory DRG neurons in nav1.6 morphants to levels found in wild type embryos (dashed black line). * and **, p

    Journal: The Journal of Neuroscience

    Article Title: BDNF mediates non cell-autonomous regulation of sensory neuron position and identity

    doi: 10.1523/JNEUROSCI.4025-10.2010

    Figure Lengend Snippet: Maintenance of DRG identity requires BDNF. A, Injection of NGF or (50 ng/mL) does not prevent the increase in migratory DRG neurons present in nav1.6 morphants (dashed grey line). In contrast, injection of BDNF or NT-3 reduces the number of migratory DRG neurons in nav1.6 morphants to levels found in wild type embryos (dashed black line). * and **, p

    Article Snippet: NGF (N-130, Alomone Labs, Israel), NT3 (N-260, Alomone Labs, Israel), or BDNF (B-250, Alomone Labs, Israel) was injected into 1.6 morphant or control Tg(−3.4neurog1:GFP) embryos at 16, 24, or 48 hpf at a concentration of 50 ng/mL.

    Techniques: Injection

    Pridopidine repairs axonal transport defects in SOD1 G93A MNs and further enhances axonal transport to a processive mode. a Schematic illustration of an experimental system for axonal transport tracking in MNs. Spinal cord (SC) explants from WT or SOD1 G93A E12.5 mouse embryos are plated in the proximal compartment of a microfluidic chamber. MNs from the spinal cord send their axons towards the distal compartment. At this point Qdot-BDNF is applied exclusively to this compartment. Axonal transport of Qdot-BDNF is then visualized and recorded by a high-resolution spinning disk confocal imaging system. b Time lapse images of Qdot-BDNF (bright orange) axonal transport as acquired at 60X magnification. Yellow arrowheads point to a single Qdot-BDNF particle that is retrogradely transported (left) towards the cell body. Scale bar: 10 µm. Bottom panel shows a kymograph of a complete Qdot-BDNF time-lapse movie. Scale bars: Horizontal 10 µm; vertical 100 s. c Bar chart of the Instantaneous Velocity values for Qdot-BDNF particles in WT (blue) or SOD1 G93A (red) MNs show slower velocities in the SOD1 G93A MNs. Pridopidine application accelerates the instantaneous velocities both in WT MNs (0.1 µM) and SOD1 G93A MNs (0.1 µM and 1 µM). Application of 25 µM or 100 µM Riluzole on SOD1 G93A MNs does not affect the instantaneous velocities. S1R − / − MNs reveal defects in the axonal transport of BDNF. Pridopidine at either 0.1 µM or 1 µM was unable to recover these defects (n = number of qDot-BDNF steps). d Bar chart of particle Stop-Count shows that pridopidine reduces the number of pauses during axonal transport in WT MNs (0.1 µM only) and SOD1 G93A MNs (both 0.1 µM and 1 µM). Axonal transport parameters of Qdot-BDNF in S1R − / − MNs show that unlike SOD G93A MNs, they are not responsive to pridopidine at any of the concentrations tested (n = number of Qdot-BDNF tracks). e , f Graphs showing the MSD over time for SOD1 G93A MNs e and S1R − / − MNs f show that pridopidine accelerates axonal transport in a S1R-dependent mechanism. g Distribution of average velocities of analyzed tracks in SOD1 G93A MNs shows a significant increase towards higher velocities in pridopidine-treated MNs. Dashed lines denote a polynomial fitting curve for each condition. Data are shown as the mean ± SEM. * p value

    Journal: Cell Death & Disease

    Article Title: Targeting the Sigma-1 Receptor via Pridopidine Ameliorates Central Features of ALS Pathology in a SOD1G93A Model

    doi: 10.1038/s41419-019-1451-2

    Figure Lengend Snippet: Pridopidine repairs axonal transport defects in SOD1 G93A MNs and further enhances axonal transport to a processive mode. a Schematic illustration of an experimental system for axonal transport tracking in MNs. Spinal cord (SC) explants from WT or SOD1 G93A E12.5 mouse embryos are plated in the proximal compartment of a microfluidic chamber. MNs from the spinal cord send their axons towards the distal compartment. At this point Qdot-BDNF is applied exclusively to this compartment. Axonal transport of Qdot-BDNF is then visualized and recorded by a high-resolution spinning disk confocal imaging system. b Time lapse images of Qdot-BDNF (bright orange) axonal transport as acquired at 60X magnification. Yellow arrowheads point to a single Qdot-BDNF particle that is retrogradely transported (left) towards the cell body. Scale bar: 10 µm. Bottom panel shows a kymograph of a complete Qdot-BDNF time-lapse movie. Scale bars: Horizontal 10 µm; vertical 100 s. c Bar chart of the Instantaneous Velocity values for Qdot-BDNF particles in WT (blue) or SOD1 G93A (red) MNs show slower velocities in the SOD1 G93A MNs. Pridopidine application accelerates the instantaneous velocities both in WT MNs (0.1 µM) and SOD1 G93A MNs (0.1 µM and 1 µM). Application of 25 µM or 100 µM Riluzole on SOD1 G93A MNs does not affect the instantaneous velocities. S1R − / − MNs reveal defects in the axonal transport of BDNF. Pridopidine at either 0.1 µM or 1 µM was unable to recover these defects (n = number of qDot-BDNF steps). d Bar chart of particle Stop-Count shows that pridopidine reduces the number of pauses during axonal transport in WT MNs (0.1 µM only) and SOD1 G93A MNs (both 0.1 µM and 1 µM). Axonal transport parameters of Qdot-BDNF in S1R − / − MNs show that unlike SOD G93A MNs, they are not responsive to pridopidine at any of the concentrations tested (n = number of Qdot-BDNF tracks). e , f Graphs showing the MSD over time for SOD1 G93A MNs e and S1R − / − MNs f show that pridopidine accelerates axonal transport in a S1R-dependent mechanism. g Distribution of average velocities of analyzed tracks in SOD1 G93A MNs shows a significant increase towards higher velocities in pridopidine-treated MNs. Dashed lines denote a polynomial fitting curve for each condition. Data are shown as the mean ± SEM. * p value

    Article Snippet: The next day, the medium in all wells was replaced with starvation medium (PNB; 1% Glutamax, 1% Penicillin-Streptomycin in Neurobasal) for 1.5 h. Fresh Quantum-dot:BDNF (Qdot-BDNF) was prepared by mixing Qdot (1 µM; Life technologies, Q10101MP) with Biotin-BDNF (30 ng/µL; Alamone Labs, B-250-B) in a 1:3 ratio.

    Techniques: Imaging

    Effects of endothelin-1 receptor blockade with tezosentan (TEZO) and nitric oxide synthase inhibition (L-NAME) on insulin-mediated vasorelaxtion of thoracic aortic rings of low-capacity running (LCR) and high-capacity running (HCR) rats. The left panels (A and B) present data from insulin dose-response curves in HCR, and right panel (C and D) present data from insulin dose-response curves in LCR. Closed circles represent % relaxation in response to insulin alone, open triangles represent % relaxation to insulin in the presence of 3 μ M TEZO a nonspecific inhibitor of ET-1 receptors (top panel, A and C) N = 9–16/group, and open squares represent % relaxation to insulin in the presence of 300 μ M L-NAME, a nitric oxide synthase inhibitor, (bottom panel, B and D) N = 6–8/group. Insulin μ IU/mL, micro-international units per milliliter. Values are expressed as means ± SEM. *Denotes line difference ( P

    Journal: Physiological Reports

    Article Title: Divergent role of nitric oxide in insulin-stimulated aortic vasorelaxation between low- and high-intrinsic aerobic capacity rats

    doi: 10.14814/phy2.12459

    Figure Lengend Snippet: Effects of endothelin-1 receptor blockade with tezosentan (TEZO) and nitric oxide synthase inhibition (L-NAME) on insulin-mediated vasorelaxtion of thoracic aortic rings of low-capacity running (LCR) and high-capacity running (HCR) rats. The left panels (A and B) present data from insulin dose-response curves in HCR, and right panel (C and D) present data from insulin dose-response curves in LCR. Closed circles represent % relaxation in response to insulin alone, open triangles represent % relaxation to insulin in the presence of 3 μ M TEZO a nonspecific inhibitor of ET-1 receptors (top panel, A and C) N = 9–16/group, and open squares represent % relaxation to insulin in the presence of 300 μ M L-NAME, a nitric oxide synthase inhibitor, (bottom panel, B and D) N = 6–8/group. Insulin μ IU/mL, micro-international units per milliliter. Values are expressed as means ± SEM. *Denotes line difference ( P

    Article Snippet: We blocked the membrane for 1 hr at room temperature with 5% nonfat milk in TBS-Tween (20 mM Tris · HCl, 137 mM NaCl, and 0.1% Tween 20), and incubated overnight at room temperature with a primary antibody against: Insulin Receptor-β (IRβ , 1:200, Santa Cruz Biotechnology, Dallas, TX); Endothelin-1 (ET-1, 1:200, Santa Cruz Biotechnology); Endothelin Receptor-A (ETA , 1:200, Sigma, St. Louis, MO); Endothelin Receptor-B (ETB, 1:250, Alamone Labs); eNOS (1:1000, Transduction Labs); and phospho-specific eNOS (1:200, Transduction Labs).

    Techniques: Inhibition

    Effects of endothelin-1 receptor blockade with tezosentan (TEZO) and nitric oxide synthase inhibition (L-NAME) on acethylcholine (ACh)-induced vasorelaxation of thoracic aortic rings of low-capacity running (LCR) and high-capacity running (HCR) rats. The left panel (A and B) present data from ACh dose-response curves in HCR, and right panel (C and D) present data from ACh dose-response curves in LCR. Closed circles represent % relaxation in response to ACh alone, open triangles represent % relaxation to ACh in the presence of 3 μ M tezosentan, a nonspecific inhibitor of ET-1 receptors (top panel, A and C) N = 9–16/group, and open squares represent % relaxation to insulin in the presence of 300 μ M L-NAME, a nitric oxide synthase inhibitor, (bottom panel, B and D) N = 6–8/group. Values are expressed as means ± SEM *Denotes line difference ( P

    Journal: Physiological Reports

    Article Title: Divergent role of nitric oxide in insulin-stimulated aortic vasorelaxation between low- and high-intrinsic aerobic capacity rats

    doi: 10.14814/phy2.12459

    Figure Lengend Snippet: Effects of endothelin-1 receptor blockade with tezosentan (TEZO) and nitric oxide synthase inhibition (L-NAME) on acethylcholine (ACh)-induced vasorelaxation of thoracic aortic rings of low-capacity running (LCR) and high-capacity running (HCR) rats. The left panel (A and B) present data from ACh dose-response curves in HCR, and right panel (C and D) present data from ACh dose-response curves in LCR. Closed circles represent % relaxation in response to ACh alone, open triangles represent % relaxation to ACh in the presence of 3 μ M tezosentan, a nonspecific inhibitor of ET-1 receptors (top panel, A and C) N = 9–16/group, and open squares represent % relaxation to insulin in the presence of 300 μ M L-NAME, a nitric oxide synthase inhibitor, (bottom panel, B and D) N = 6–8/group. Values are expressed as means ± SEM *Denotes line difference ( P

    Article Snippet: We blocked the membrane for 1 hr at room temperature with 5% nonfat milk in TBS-Tween (20 mM Tris · HCl, 137 mM NaCl, and 0.1% Tween 20), and incubated overnight at room temperature with a primary antibody against: Insulin Receptor-β (IRβ , 1:200, Santa Cruz Biotechnology, Dallas, TX); Endothelin-1 (ET-1, 1:200, Santa Cruz Biotechnology); Endothelin Receptor-A (ETA , 1:200, Sigma, St. Louis, MO); Endothelin Receptor-B (ETB, 1:250, Alamone Labs); eNOS (1:1000, Transduction Labs); and phospho-specific eNOS (1:200, Transduction Labs).

    Techniques: Inhibition