α conotoxin imi  (Alomone Labs)


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    Alomone Labs α conotoxin imi
    α Conotoxin Imi, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/α conotoxin imi/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    α conotoxin imi - by Bioz Stars, 2023-02
    94/100 stars

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    α conotoxin imi  (Alomone Labs)


    Bioz Verified Symbol Alomone Labs is a verified supplier
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    Structured Review

    Alomone Labs α conotoxin imi
    α Conotoxin Imi, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/α conotoxin imi/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    α conotoxin imi - by Bioz Stars, 2023-02
    94/100 stars

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    α conotoxin imi  (Alomone Labs)


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    Structured Review

    Alomone Labs α conotoxin imi
    Effect of nicotinic receptor agonists and antagonists on transepithelial ion transport of mouse tracheal epithelium. (a) The α7 nicotinic ACh receptor (nAChR) antagonist α‐bungarotoxin (αBTX, 100 nmol·L −1 , n = 5, apical) or the α7 nAChR antagonist <t>α‐conotoxin</t> ImI (C. ImI, 4 μmol·L −1 , apical) or the α9α10 nAChR antagonist ACV‐1 (100 nmol·L −1 , apical) did not influence the nicotine effect (100 μmol·L −1 , apical, ΔI SC ; ns, not significant). (b) The epibatidine‐induced (α4β2, α3β2, α4β4 and α3β4 nAChR agonist) current peak (1 μmol·L −1 ) was significant compared to baseline current ( n = 5, * P < 0.05). Application of the α4β2 and α3β4 nAChR agonist A‐85380 (100 μmol·L −1 , apical, n = 5) significantly increased I SC (* P < 0.05). (c) The epibatidine effect was dose dependent ( n = 5 for each concentration). (d) In the presence of 1 μmol·L −1 of the α4β2, α3β2, α4β4 and α3β4 nAChR antagonist dihydro‐β‐erythroidine (DhβE), the nicotine effect (ΔI SC ) was similar to control conditions ( n = 5; ns, not significant), but 10 μmol·L −1 DhβE significantly reduced the nicotine‐induced current (ΔI SC , n = 5, * P < 0.05). (e) The α3β2 nAChR antagonist α‐conotoxin MII (C. MII) did not influence the nicotine effect (ΔI SC ) in a concentration of 50 nmol·L −1 ( n = 5; ns, not significant) but significantly reduced the nicotine‐induced current (ΔI SC , n = 5, * P < 0.05) in a concentration of 1 μmol·L −1 . (f) The α3β2 antagonist α‐conotoxin PnIA (C. PnIA) did not influence the nicotine effect (ΔI SC ) in a concentration of 100 nmol·L −1 ( n = 6; ns, not significant) but significantly reduced the nicotine‐induced current in a concentration of 500 mmol·L −1 (ΔI SC , n = 5, * P < 0.05)
    α Conotoxin Imi, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/α conotoxin imi/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    α conotoxin imi - by Bioz Stars, 2023-02
    94/100 stars

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    1) Product Images from "Nicotine stimulates ion transport via metabotropic β4 subunit containing nicotinic ACh receptors"

    Article Title: Nicotine stimulates ion transport via metabotropic β4 subunit containing nicotinic ACh receptors

    Journal: British Journal of Pharmacology

    doi: 10.1111/bph.15270

    Effect of nicotinic receptor agonists and antagonists on transepithelial ion transport of mouse tracheal epithelium. (a) The α7 nicotinic ACh receptor (nAChR) antagonist α‐bungarotoxin (αBTX, 100 nmol·L −1 , n = 5, apical) or the α7 nAChR antagonist α‐conotoxin ImI (C. ImI, 4 μmol·L −1 , apical) or the α9α10 nAChR antagonist ACV‐1 (100 nmol·L −1 , apical) did not influence the nicotine effect (100 μmol·L −1 , apical, ΔI SC ; ns, not significant). (b) The epibatidine‐induced (α4β2, α3β2, α4β4 and α3β4 nAChR agonist) current peak (1 μmol·L −1 ) was significant compared to baseline current ( n = 5, * P < 0.05). Application of the α4β2 and α3β4 nAChR agonist A‐85380 (100 μmol·L −1 , apical, n = 5) significantly increased I SC (* P < 0.05). (c) The epibatidine effect was dose dependent ( n = 5 for each concentration). (d) In the presence of 1 μmol·L −1 of the α4β2, α3β2, α4β4 and α3β4 nAChR antagonist dihydro‐β‐erythroidine (DhβE), the nicotine effect (ΔI SC ) was similar to control conditions ( n = 5; ns, not significant), but 10 μmol·L −1 DhβE significantly reduced the nicotine‐induced current (ΔI SC , n = 5, * P < 0.05). (e) The α3β2 nAChR antagonist α‐conotoxin MII (C. MII) did not influence the nicotine effect (ΔI SC ) in a concentration of 50 nmol·L −1 ( n = 5; ns, not significant) but significantly reduced the nicotine‐induced current (ΔI SC , n = 5, * P < 0.05) in a concentration of 1 μmol·L −1 . (f) The α3β2 antagonist α‐conotoxin PnIA (C. PnIA) did not influence the nicotine effect (ΔI SC ) in a concentration of 100 nmol·L −1 ( n = 6; ns, not significant) but significantly reduced the nicotine‐induced current in a concentration of 500 mmol·L −1 (ΔI SC , n = 5, * P < 0.05)
    Figure Legend Snippet: Effect of nicotinic receptor agonists and antagonists on transepithelial ion transport of mouse tracheal epithelium. (a) The α7 nicotinic ACh receptor (nAChR) antagonist α‐bungarotoxin (αBTX, 100 nmol·L −1 , n = 5, apical) or the α7 nAChR antagonist α‐conotoxin ImI (C. ImI, 4 μmol·L −1 , apical) or the α9α10 nAChR antagonist ACV‐1 (100 nmol·L −1 , apical) did not influence the nicotine effect (100 μmol·L −1 , apical, ΔI SC ; ns, not significant). (b) The epibatidine‐induced (α4β2, α3β2, α4β4 and α3β4 nAChR agonist) current peak (1 μmol·L −1 ) was significant compared to baseline current ( n = 5, * P < 0.05). Application of the α4β2 and α3β4 nAChR agonist A‐85380 (100 μmol·L −1 , apical, n = 5) significantly increased I SC (* P < 0.05). (c) The epibatidine effect was dose dependent ( n = 5 for each concentration). (d) In the presence of 1 μmol·L −1 of the α4β2, α3β2, α4β4 and α3β4 nAChR antagonist dihydro‐β‐erythroidine (DhβE), the nicotine effect (ΔI SC ) was similar to control conditions ( n = 5; ns, not significant), but 10 μmol·L −1 DhβE significantly reduced the nicotine‐induced current (ΔI SC , n = 5, * P < 0.05). (e) The α3β2 nAChR antagonist α‐conotoxin MII (C. MII) did not influence the nicotine effect (ΔI SC ) in a concentration of 50 nmol·L −1 ( n = 5; ns, not significant) but significantly reduced the nicotine‐induced current (ΔI SC , n = 5, * P < 0.05) in a concentration of 1 μmol·L −1 . (f) The α3β2 antagonist α‐conotoxin PnIA (C. PnIA) did not influence the nicotine effect (ΔI SC ) in a concentration of 100 nmol·L −1 ( n = 6; ns, not significant) but significantly reduced the nicotine‐induced current in a concentration of 500 mmol·L −1 (ΔI SC , n = 5, * P < 0.05)

    Techniques Used: Concentration Assay

    α ltx  (Alomone Labs)


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    Alomone Labs α ltx
    NUCC-390 promotes functional and anatomical recovery of the NMJ. ( A ) Mice locally injected in the left hind limb with <t>α-LTx</t> were daily treated either with vehicle, or NUCC-390, or AMD3100, or their combinations. Seventy-two hours later, soleus muscles were dissected, and EJPs recorded. * p < 0.05, ** p < 0.01; ns = not significant. Bars represent mean ± SEM from 4 mice, 15 fibers analyzed/muscle. ( B ) The same muscles in A were paraformaldehyde (PFA)-fixed, and the neuromuscular junction (NMJ) stained for the presynaptic marker syntaxin-1A/1B (green), and for acetylcholine receptors (nAChR) by fluorescent α-BTx (red). Scale bars: 100 µm. Yellow signals in merge panels correspond to regenerated NMJ. White asterisks indicate still degenerated NMJ. Panels on the right display representative fields at higher magnification. Scale bars: 50 µm. ( C ) Quantitative analysis of degenerated NMJ in soleus muscles after α-LTx-induced injury ± treatments reported as a percentage of vehicle-treated mice. Bars represent mean ± SEM from 4 animals. *** p < 0.001. ns = not significant.
    α Ltx, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/α ltx/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    α ltx - by Bioz Stars, 2023-02
    94/100 stars

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    1) Product Images from "An Agonist of the CXCR4 Receptor Strongly Promotes Regeneration of Degenerated Motor Axon Terminals"

    Article Title: An Agonist of the CXCR4 Receptor Strongly Promotes Regeneration of Degenerated Motor Axon Terminals

    Journal: Cells

    doi: 10.3390/cells8101183

    NUCC-390 promotes functional and anatomical recovery of the NMJ. ( A ) Mice locally injected in the left hind limb with α-LTx were daily treated either with vehicle, or NUCC-390, or AMD3100, or their combinations. Seventy-two hours later, soleus muscles were dissected, and EJPs recorded. * p < 0.05, ** p < 0.01; ns = not significant. Bars represent mean ± SEM from 4 mice, 15 fibers analyzed/muscle. ( B ) The same muscles in A were paraformaldehyde (PFA)-fixed, and the neuromuscular junction (NMJ) stained for the presynaptic marker syntaxin-1A/1B (green), and for acetylcholine receptors (nAChR) by fluorescent α-BTx (red). Scale bars: 100 µm. Yellow signals in merge panels correspond to regenerated NMJ. White asterisks indicate still degenerated NMJ. Panels on the right display representative fields at higher magnification. Scale bars: 50 µm. ( C ) Quantitative analysis of degenerated NMJ in soleus muscles after α-LTx-induced injury ± treatments reported as a percentage of vehicle-treated mice. Bars represent mean ± SEM from 4 animals. *** p < 0.001. ns = not significant.
    Figure Legend Snippet: NUCC-390 promotes functional and anatomical recovery of the NMJ. ( A ) Mice locally injected in the left hind limb with α-LTx were daily treated either with vehicle, or NUCC-390, or AMD3100, or their combinations. Seventy-two hours later, soleus muscles were dissected, and EJPs recorded. * p < 0.05, ** p < 0.01; ns = not significant. Bars represent mean ± SEM from 4 mice, 15 fibers analyzed/muscle. ( B ) The same muscles in A were paraformaldehyde (PFA)-fixed, and the neuromuscular junction (NMJ) stained for the presynaptic marker syntaxin-1A/1B (green), and for acetylcholine receptors (nAChR) by fluorescent α-BTx (red). Scale bars: 100 µm. Yellow signals in merge panels correspond to regenerated NMJ. White asterisks indicate still degenerated NMJ. Panels on the right display representative fields at higher magnification. Scale bars: 50 µm. ( C ) Quantitative analysis of degenerated NMJ in soleus muscles after α-LTx-induced injury ± treatments reported as a percentage of vehicle-treated mice. Bars represent mean ± SEM from 4 animals. *** p < 0.001. ns = not significant.

    Techniques Used: Functional Assay, Injection, Staining, Marker

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    • α conotoxin imi  (Alomone Labs)
    94
    Alomone Labs α conotoxin imi
    α Conotoxin Imi, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/α conotoxin imi/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    α conotoxin imi - by Bioz Stars, 2023-02
    94/100 stars
    		  Buy from Supplier
    α ltx  (Alomone Labs)
    94
    Alomone Labs α ltx
    NUCC-390 promotes functional and anatomical recovery of the NMJ. ( A ) Mice locally injected in the left hind limb with <t>α-LTx</t> were daily treated either with vehicle, or NUCC-390, or AMD3100, or their combinations. Seventy-two hours later, soleus muscles were dissected, and EJPs recorded. * p < 0.05, ** p < 0.01; ns = not significant. Bars represent mean ± SEM from 4 mice, 15 fibers analyzed/muscle. ( B ) The same muscles in A were paraformaldehyde (PFA)-fixed, and the neuromuscular junction (NMJ) stained for the presynaptic marker syntaxin-1A/1B (green), and for acetylcholine receptors (nAChR) by fluorescent α-BTx (red). Scale bars: 100 µm. Yellow signals in merge panels correspond to regenerated NMJ. White asterisks indicate still degenerated NMJ. Panels on the right display representative fields at higher magnification. Scale bars: 50 µm. ( C ) Quantitative analysis of degenerated NMJ in soleus muscles after α-LTx-induced injury ± treatments reported as a percentage of vehicle-treated mice. Bars represent mean ± SEM from 4 animals. *** p < 0.001. ns = not significant.
    α Ltx, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/α ltx/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    α ltx - by Bioz Stars, 2023-02
    94/100 stars
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    NUCC-390 promotes functional and anatomical recovery of the NMJ. ( A ) Mice locally injected in the left hind limb with α-LTx were daily treated either with vehicle, or NUCC-390, or AMD3100, or their combinations. Seventy-two hours later, soleus muscles were dissected, and EJPs recorded. * p < 0.05, ** p < 0.01; ns = not significant. Bars represent mean ± SEM from 4 mice, 15 fibers analyzed/muscle. ( B ) The same muscles in A were paraformaldehyde (PFA)-fixed, and the neuromuscular junction (NMJ) stained for the presynaptic marker syntaxin-1A/1B (green), and for acetylcholine receptors (nAChR) by fluorescent α-BTx (red). Scale bars: 100 µm. Yellow signals in merge panels correspond to regenerated NMJ. White asterisks indicate still degenerated NMJ. Panels on the right display representative fields at higher magnification. Scale bars: 50 µm. ( C ) Quantitative analysis of degenerated NMJ in soleus muscles after α-LTx-induced injury ± treatments reported as a percentage of vehicle-treated mice. Bars represent mean ± SEM from 4 animals. *** p < 0.001. ns = not significant.

    Journal: Cells

    Article Title: An Agonist of the CXCR4 Receptor Strongly Promotes Regeneration of Degenerated Motor Axon Terminals

    doi: 10.3390/cells8101183

    Figure Lengend Snippet: NUCC-390 promotes functional and anatomical recovery of the NMJ. ( A ) Mice locally injected in the left hind limb with α-LTx were daily treated either with vehicle, or NUCC-390, or AMD3100, or their combinations. Seventy-two hours later, soleus muscles were dissected, and EJPs recorded. * p < 0.05, ** p < 0.01; ns = not significant. Bars represent mean ± SEM from 4 mice, 15 fibers analyzed/muscle. ( B ) The same muscles in A were paraformaldehyde (PFA)-fixed, and the neuromuscular junction (NMJ) stained for the presynaptic marker syntaxin-1A/1B (green), and for acetylcholine receptors (nAChR) by fluorescent α-BTx (red). Scale bars: 100 µm. Yellow signals in merge panels correspond to regenerated NMJ. White asterisks indicate still degenerated NMJ. Panels on the right display representative fields at higher magnification. Scale bars: 50 µm. ( C ) Quantitative analysis of degenerated NMJ in soleus muscles after α-LTx-induced injury ± treatments reported as a percentage of vehicle-treated mice. Bars represent mean ± SEM from 4 animals. *** p < 0.001. ns = not significant.

    Article Snippet: Cytosine β- d -arabinofuranoside hydrochloride (C6645), DNase I from bovine pancreas (DN25), poly- l -lysine hydrobromide (P1274), laminin (L2020) and trypsin (T4799) were from Sigma–Aldrich (Milan, Italy). µ-Conotoxin GIIIB and α-LTx were purchased from Alomone (Jerusalem, Israel).

    Techniques: Functional Assay, Injection, Staining, Marker