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cgrp  (Tocris)


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    Structured Review

    Tocris cgrp
    Cgrp, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cgrp/CGRP+(rat)/pmc02707992-156-0-2
    Average 91 stars, based on 27 article reviews
    cgrp - by Bioz Stars, 2026-11
    91/100 stars

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    Related Articles

    Saline:

    Article Title: Calcitonin gene-related peptide and its receptor plays important role in nociceptive regulation in the arcuate nucleus of hypothalamus of rats with inflammatory pain.
    Article Snippet: The present study has explored the role of calcitonin gene-related peptide (CGRP) and its receptor in inflammatory pain modulation in arcuate nucleus of hypothalamus (ARC).. Our study demonstrated that intra-ARC injection of CGRP induced antinociceptive effects to naïve rats and rats with inflammatory pain, the effect could be inhibited by the selective CGRP receptor antagonist CGRP8–37.. Interestingly, the CGRP-induced antinociception effect was decreased in rats with inflammatory pain compared to naïve rats.

    other:

    Article Title: Lidocaine Ameliorates Psoriasis by Obstructing Pathogenic CGRP Signaling‒Mediated Sensory Neuron‒Dendritic Cell Communication.
    Article Snippet: Psoriasis is a chronic immune-mediated skin disorder with the nervous system contributing to its pathology.. The neurogenic mediators of psoriasis are elusive, and whether the intervention of the cutaneous nervous system can treat psoriasis remains to be determined.. In this study, we conducted a pilot study using an epidural injection of lidocaine to treat patients with psoriasis.

    Article Title: Acetaminophen (Paracetamol) metabolites induce vasodilation and hypotension by activating Kv7 potassium channels directly and indirectly
    Article Snippet: Chemicals and Reagents Paracetamol (acetaminophen, APAP), N-arachidonoylaminophenol (AM404), N-acetyl-p-benzoquinone imine (NAPQI), linopirdine, methoxamine, indomethacin and capsaicin were purchased from Sigma-Aldrich (Søborg, DK).

    Injection:

    Article Title: Sensory ASIC3 channel exacerbates psoriatic inflammation via a neurogenic pathway in female mice
    Article Snippet: To treat Asic3 +/+ mice, a daily subcutaneous administration of 10 μg BIBN4096 (Tocris, Catalog no. 4561) was delivered to the anticipated inflamed dorsal skin and the same volume of PBS was injected as a control. .. To examine the effects of CGRP on psoriatic inflammation, a daily subcutaneous injection of 0.5 μg CGRP (Tocris, Catalog no. 1161) was made to the anticipated inflamed site in dorsal skin of Asic3 −/− mice. ..



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    Generation of iPSC line BO-VC1 -derived nociceptive neurons. Differentiation of ( A ) human iPSC line BO-VC1 into nociceptive neurons was done by dual SMAD inhibition, suppressing TGF-ß and BMP4 signaling, in knockout serum replacement (KSR) medium (day 0–4). This was followed by an overlapping inhibition of glycogen synthase kinase-3ß (GSK-3ß), vascular endothelial growth factor (VEGF), and Notch signaling (day 2–12), with KSR medium incremented with N2/B27 medium every second day by 25% from day 4 on. After reseeding of the ( B ) immature sensory neurons, final maturation was performed in N2/B27 medium infused with the neurotrophic factors glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) (day 13 - approx. 60) according to the protocols of Chambers and Schoepf leading to the differentiation of ( C ) intermediate and finally ( D ) mature nociceptors (Scale bar: 500 μm). Mature nociceptive neurons express ( E ) the neuron specific microtubule element βIII-tubulin (βIIITUB) and vGLUT2, the sensory neuron markers ( F ) insulin gene enhancer protein 1 (ISL1) as well as the brain-specific homeobox/POU domain protein 3 A (BRN3A). Additionally, iPSC-derived differentiated cells express the nociceptive markers ( G ) transient receptor potential cation channel subfamily V member 1(TRPV1), H voltage-gated sodium ion channel 1.9 (Na V 1.9) and I TWIK-related spinal cord potassium channel (TRESK). Moreover, co-expression of ( J ) the calcitonin gene-related peptide <t>(CGRP),</t> the nociceptive marker high affinity nerve growth factor <t>receptor</t> <t>(TRKA)</t> and the estrogen receptor G-protein coupled estrogen receptor 1 (GPER1) was confirmed (Scale bars: 50 μm) ( K ) Quantification of the percentage of positive cells for the respective markers was 95.96 ± 2,495% for CGRP, 89.68 ± 6,137% for GPER1, 91.67 ± 5.270% for Na V 1.9, 95.83 ± 4.167% for TRKA, 80.38 ± 7.143% for TRPV1 and 98.55 ± 0.2899% for TRESK. L Realtime-PCR analysis in order to quantify nociceptive neuron marker and GPER1 gene expression of HDFa-derived iPSCs (line BO-VC1) and corresponding nociceptive neurons relative to HDFa cell samples mean value. Means ± SEM (standard error of the mean) from three independent passages were statistically analyzed by one-way ANOVA with Turkey’s multiple comparison test (L). n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)
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    Generation of iPSC line BO-VC1 -derived nociceptive neurons. Differentiation of ( A ) human iPSC line BO-VC1 into nociceptive neurons was done by dual SMAD inhibition, suppressing TGF-ß and BMP4 signaling, in knockout serum replacement (KSR) medium (day 0–4). This was followed by an overlapping inhibition of glycogen synthase kinase-3ß (GSK-3ß), vascular endothelial growth factor (VEGF), and Notch signaling (day 2–12), with KSR medium incremented with N2/B27 medium every second day by 25% from day 4 on. After reseeding of the ( B ) immature sensory neurons, final maturation was performed in N2/B27 medium infused with the neurotrophic factors glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) (day 13 - approx. 60) according to the protocols of Chambers and Schoepf leading to the differentiation of ( C ) intermediate and finally ( D ) mature nociceptors (Scale bar: 500 μm). Mature nociceptive neurons express ( E ) the neuron specific microtubule element βIII-tubulin (βIIITUB) and vGLUT2, the sensory neuron markers ( F ) insulin gene enhancer protein 1 (ISL1) as well as the brain-specific homeobox/POU domain protein 3 A (BRN3A). Additionally, iPSC-derived differentiated cells express the nociceptive markers ( G ) transient receptor potential cation channel subfamily V member 1(TRPV1), H voltage-gated sodium ion channel 1.9 (Na V 1.9) and I TWIK-related spinal cord potassium channel (TRESK). Moreover, co-expression of ( J ) the calcitonin gene-related peptide <t>(CGRP),</t> the nociceptive marker high affinity nerve growth factor <t>receptor</t> <t>(TRKA)</t> and the estrogen receptor G-protein coupled estrogen receptor 1 (GPER1) was confirmed (Scale bars: 50 μm) ( K ) Quantification of the percentage of positive cells for the respective markers was 95.96 ± 2,495% for CGRP, 89.68 ± 6,137% for GPER1, 91.67 ± 5.270% for Na V 1.9, 95.83 ± 4.167% for TRKA, 80.38 ± 7.143% for TRPV1 and 98.55 ± 0.2899% for TRESK. L Realtime-PCR analysis in order to quantify nociceptive neuron marker and GPER1 gene expression of HDFa-derived iPSCs (line BO-VC1) and corresponding nociceptive neurons relative to HDFa cell samples mean value. Means ± SEM (standard error of the mean) from three independent passages were statistically analyzed by one-way ANOVA with Turkey’s multiple comparison test (L). n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)
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    Generation of iPSC line BO-VC1 -derived nociceptive neurons. Differentiation of ( A ) human iPSC line BO-VC1 into nociceptive neurons was done by dual SMAD inhibition, suppressing TGF-ß and BMP4 signaling, in knockout serum replacement (KSR) medium (day 0–4). This was followed by an overlapping inhibition of glycogen synthase kinase-3ß (GSK-3ß), vascular endothelial growth factor (VEGF), and Notch signaling (day 2–12), with KSR medium incremented with N2/B27 medium every second day by 25% from day 4 on. After reseeding of the ( B ) immature sensory neurons, final maturation was performed in N2/B27 medium infused with the neurotrophic factors glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) (day 13 - approx. 60) according to the protocols of Chambers and Schoepf leading to the differentiation of ( C ) intermediate and finally ( D ) mature nociceptors (Scale bar: 500 μm). Mature nociceptive neurons express ( E ) the neuron specific microtubule element βIII-tubulin (βIIITUB) and vGLUT2, the sensory neuron markers ( F ) insulin gene enhancer protein 1 (ISL1) as well as the brain-specific homeobox/POU domain protein 3 A (BRN3A). Additionally, iPSC-derived differentiated cells express the nociceptive markers ( G ) transient receptor potential cation channel subfamily V member 1(TRPV1), H voltage-gated sodium ion channel 1.9 (Na V 1.9) and I TWIK-related spinal cord potassium channel (TRESK). Moreover, co-expression of ( J ) the calcitonin gene-related peptide <t>(CGRP),</t> the nociceptive marker high affinity nerve growth factor <t>receptor</t> <t>(TRKA)</t> and the estrogen receptor G-protein coupled estrogen receptor 1 (GPER1) was confirmed (Scale bars: 50 μm) ( K ) Quantification of the percentage of positive cells for the respective markers was 95.96 ± 2,495% for CGRP, 89.68 ± 6,137% for GPER1, 91.67 ± 5.270% for Na V 1.9, 95.83 ± 4.167% for TRKA, 80.38 ± 7.143% for TRPV1 and 98.55 ± 0.2899% for TRESK. L Realtime-PCR analysis in order to quantify nociceptive neuron marker and GPER1 gene expression of HDFa-derived iPSCs (line BO-VC1) and corresponding nociceptive neurons relative to HDFa cell samples mean value. Means ± SEM (standard error of the mean) from three independent passages were statistically analyzed by one-way ANOVA with Turkey’s multiple comparison test (L). n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)
    Ratio Cgrp Abclonal A5542, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Journal: Cell Reports Medicine

    Article Title: A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration

    doi: 10.1016/j.xcrm.2026.102937

    Figure Lengend Snippet:

    Article Snippet: Rabbit Polyclonal anti-CGRP , ABclonal , Cat# A5542; RRID: AB_2766323.

    Techniques: Recombinant, Lysis, Hydroxyproline Assay, Enzyme-linked Immunosorbent Assay, Isolation, SYBR Green Assay, Bicinchoninic Acid Protein Assay, Staining, Software

    Generation of iPSC line BO-VC1 -derived nociceptive neurons. Differentiation of ( A ) human iPSC line BO-VC1 into nociceptive neurons was done by dual SMAD inhibition, suppressing TGF-ß and BMP4 signaling, in knockout serum replacement (KSR) medium (day 0–4). This was followed by an overlapping inhibition of glycogen synthase kinase-3ß (GSK-3ß), vascular endothelial growth factor (VEGF), and Notch signaling (day 2–12), with KSR medium incremented with N2/B27 medium every second day by 25% from day 4 on. After reseeding of the ( B ) immature sensory neurons, final maturation was performed in N2/B27 medium infused with the neurotrophic factors glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) (day 13 - approx. 60) according to the protocols of Chambers and Schoepf leading to the differentiation of ( C ) intermediate and finally ( D ) mature nociceptors (Scale bar: 500 μm). Mature nociceptive neurons express ( E ) the neuron specific microtubule element βIII-tubulin (βIIITUB) and vGLUT2, the sensory neuron markers ( F ) insulin gene enhancer protein 1 (ISL1) as well as the brain-specific homeobox/POU domain protein 3 A (BRN3A). Additionally, iPSC-derived differentiated cells express the nociceptive markers ( G ) transient receptor potential cation channel subfamily V member 1(TRPV1), H voltage-gated sodium ion channel 1.9 (Na V 1.9) and I TWIK-related spinal cord potassium channel (TRESK). Moreover, co-expression of ( J ) the calcitonin gene-related peptide (CGRP), the nociceptive marker high affinity nerve growth factor receptor (TRKA) and the estrogen receptor G-protein coupled estrogen receptor 1 (GPER1) was confirmed (Scale bars: 50 μm) ( K ) Quantification of the percentage of positive cells for the respective markers was 95.96 ± 2,495% for CGRP, 89.68 ± 6,137% for GPER1, 91.67 ± 5.270% for Na V 1.9, 95.83 ± 4.167% for TRKA, 80.38 ± 7.143% for TRPV1 and 98.55 ± 0.2899% for TRESK. L Realtime-PCR analysis in order to quantify nociceptive neuron marker and GPER1 gene expression of HDFa-derived iPSCs (line BO-VC1) and corresponding nociceptive neurons relative to HDFa cell samples mean value. Means ± SEM (standard error of the mean) from three independent passages were statistically analyzed by one-way ANOVA with Turkey’s multiple comparison test (L). n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)

    Journal: Stem Cell Research & Therapy

    Article Title: Activation of the G-protein coupled estrogen receptor 1 (GPER1) reduces transient receptor potential vanilloid 1 (TRPV1) activity and human iPSC-derived nociceptive neuron firing

    doi: 10.1186/s13287-026-05174-3

    Figure Lengend Snippet: Generation of iPSC line BO-VC1 -derived nociceptive neurons. Differentiation of ( A ) human iPSC line BO-VC1 into nociceptive neurons was done by dual SMAD inhibition, suppressing TGF-ß and BMP4 signaling, in knockout serum replacement (KSR) medium (day 0–4). This was followed by an overlapping inhibition of glycogen synthase kinase-3ß (GSK-3ß), vascular endothelial growth factor (VEGF), and Notch signaling (day 2–12), with KSR medium incremented with N2/B27 medium every second day by 25% from day 4 on. After reseeding of the ( B ) immature sensory neurons, final maturation was performed in N2/B27 medium infused with the neurotrophic factors glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) (day 13 - approx. 60) according to the protocols of Chambers and Schoepf leading to the differentiation of ( C ) intermediate and finally ( D ) mature nociceptors (Scale bar: 500 μm). Mature nociceptive neurons express ( E ) the neuron specific microtubule element βIII-tubulin (βIIITUB) and vGLUT2, the sensory neuron markers ( F ) insulin gene enhancer protein 1 (ISL1) as well as the brain-specific homeobox/POU domain protein 3 A (BRN3A). Additionally, iPSC-derived differentiated cells express the nociceptive markers ( G ) transient receptor potential cation channel subfamily V member 1(TRPV1), H voltage-gated sodium ion channel 1.9 (Na V 1.9) and I TWIK-related spinal cord potassium channel (TRESK). Moreover, co-expression of ( J ) the calcitonin gene-related peptide (CGRP), the nociceptive marker high affinity nerve growth factor receptor (TRKA) and the estrogen receptor G-protein coupled estrogen receptor 1 (GPER1) was confirmed (Scale bars: 50 μm) ( K ) Quantification of the percentage of positive cells for the respective markers was 95.96 ± 2,495% for CGRP, 89.68 ± 6,137% for GPER1, 91.67 ± 5.270% for Na V 1.9, 95.83 ± 4.167% for TRKA, 80.38 ± 7.143% for TRPV1 and 98.55 ± 0.2899% for TRESK. L Realtime-PCR analysis in order to quantify nociceptive neuron marker and GPER1 gene expression of HDFa-derived iPSCs (line BO-VC1) and corresponding nociceptive neurons relative to HDFa cell samples mean value. Means ± SEM (standard error of the mean) from three independent passages were statistically analyzed by one-way ANOVA with Turkey’s multiple comparison test (L). n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)

    Article Snippet: Nevertheless, incubation with the first antibodies CGRP (1:500; # 414 004, Synaptic Systems GmbH, Göttingen, Germany), TRKA (1:500; # MA515509 , Thermo Fisher Scientific, Darmstadt, Germany), GPER1 (1:500; # ab39742, Abcam, ), BRN3A (1:100, # ab245230, Abcam, Cambridge, UK), ISL1 (1:100, #H00003670-M05, Abnova, Taipeh, Taiwan), TRPV1 (1:1000, # SAB5700857, Sigma-Aldrich, Merck, Darmstadt, Germany), vGlut2 (1:400, # MAB5504, Sigma-Aldrich, Merck, Darmstadt, Germany), ßIIITUB (1:300, # PA1-41331, Thermo Fisher Scientific, Darmstadt, Germany or 1:250, #302 304, Synaptic Systems GmbH, Göttingen, Germany) and Na V 1.9 (1:100, # ab65160, Abcam, Cambridge, UK) was done at 4 °C overnight.

    Techniques: Derivative Assay, Inhibition, Knock-Out, Expressing, Marker, Gene Expression, Comparison