α7nachr

Manufactured by Jackson ImmunoResearch

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α7nAChR is a nicotinic acetylcholine receptor subunit that forms part of the ligand-gated ion channel. It is involved in the regulation of neuronal signaling and synaptic transmission.

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Lab products found in correlation

B6 cg chrna7tm1.1ehs yakelj, by Jackson ImmunoResearch (1 mentions) Mightyamp genotyping kit, by Takara Bio (1 mentions) Lps from escherichia coli o111 b4, by Merck Group (1 mentions) Rag1 mice b6.129s7 rag1tm1mom j, by Jackson ImmunoResearch (1 mentions) Nicotine, by Merck Group (1 mentions) Salbutamol, by Merck Group (1 mentions) Butoxamine, by Merck Group (1 mentions)

4 protocols using α7nachr

Genetically Modified Mice for Bone Research

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α7nAChR knockout (α7nAChR^−/−, background, C57BL/6J, B6.129S7-Chrna7tm1Bay/J, stock no. 003232) and Akt1^−/−mice (backcrossed to a C57BL/6 background for 6 generations) were purchased from Jackson Laboratory (Bar Harbor, ME, USA) [2 (link)]. Littermate wild-type mice (C57BL/6J background, 6–8 weeks old) were used as controls. We only used male mice in the study considering that estrogen in females may influence the effect of the bone marrow-derived progenitor cells [34 (link)]. The mice were housed with free access to food and water in 12-h dark/light cycle. Anesthetization was performed by intraperitoneal injection of pentobarbital sodium (50 mg/kg). The protocols were approved by the Committees on Animal Research of the Institut Pasteur of Shanghai, Chinese Academy of Sciences, China.

Chen X., Chen J., Song Y, & Su X. (2020). Vagal α7nAChR signaling regulates α7nAChR+Sca1+ cells during lung injury repair. Stem Cell Research & Therapy, 11, 375.

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Generation of Macrophage-Specific α7nAChR KO Mice

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C57BL/6 J male mice (8–12 weeks old, 20–25 g) purchased from CLEA (Tokyo, Japan) were used as WT mice. To generate macrophage-specific α7nAChR KO mice, lysozyme M (LysM)-Cre and α7nAChR ^flox/flox (B6(Cg)-Chrna7^tm1.1Ehs/YakelJ, Jackson Laboratory, Bar Harbor, ME, USA) mice were crossbred for several generations. LysM-Cre: α7 flox mice were genotyped using tail PCR based on the protocol provided by the Jackson Laboratory using a MightyAmp Genotyping kit (Takara Bio Inc., Shiga, Japan). The primer sequence used in tail-PCR is listed in Supplementary Table 1. LysM-Cre: α7 flox male and female mice (8–18 weeks old) were used for the experiments. General anesthesia (0.3 mg kg⁻¹ medetomidine, 5 mg kg⁻¹ butorphanol, and 4 mg kg⁻¹ midazolam) was administered for all surgeries and euthanasia.

Nakamura Y., Matsumoto H., Wu C.H., Fukaya D., Uni R., Hirakawa Y., Katagiri M., Yamada S., Ko T., Nomura S., Wada Y., Komuro I., Nangaku M., Inagi R, & Inoue T. (2023). Alpha 7 nicotinic acetylcholine receptors signaling boosts cell-cell interactions in macrophages effecting anti-inflammatory and organ protection. Communications Biology, 6, 666.

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Pharmacological Modulation of α7nAChR in Mice

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Male mice (8–12 weeks of age, 20–25 g) were used for all experiments. Wild-type C57Bl/6 mice were purchased from the National Cancer Institute (Frederick, MD), α7nAChR^−/− mice (B6.129S7-Chrna7tm1Bay/J) were obtained from Jackson Laboratories (Bar Harbor, ME), and WT (α7nAChR^+/+) progeny were used as controls in Figures 1 and 2. Rag1^−/− mice (B6.129S7-Rag1tm1Mom/J) were obtained from Jackson Laboratories. Butoxamine (β2-adrenergic receptor antagonist), salbutamol (β2-adrenergic receptor agonist), nicotine (nicotinic acetylcholine receptor agonist), and LPS (from Escherichia coli O111:B4) were purchased from Sigma-Aldrich (St. Louis, MO).

Inoue T., Abe C., Kohro T., Tanaka S., Huang L., Yao J., Zheng S., Ye H., Inagi R., Stornetta R.L., Rosin D.L., Nangaku M., Wada Y, & Okusa M.D. (2019). Non-canonical cholinergic anti-inflammatory pathway-mediated activation of peritoneal macrophages induces Hes1 and blocks ischemia/reperfusion injury in the kidney. Kidney international, 95(3), 563-576.

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Myocardial Ischemia-Reperfusion Injury in Mice

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C57BL/6 wild type (WT) mice and α7-nicotinic acetylcholine
receptor knockout (α7nAChR^−/−) mice (both
9–11 weeks, purchased from The Jackson Laboratory, Bar Harbor, ME) were
used in the study. For myocardial IRI experiments, all mice underwent the IRI
procedure described below (n=5–10 per group). Acute hyperglycemia (HG)
was induced by intraperitoneal injection of 20% glucose (10 μL/g body
weight) 15 minutes before occlusion of the left coronary artery (LCA). Blood
glucose levels were monitored with a conventional glucometer (Auto Control Med,
Inc., Canada) via tail venipuncture. Groups were further differentiated by
treatment with or without pUS or control B-mode ultrasound (BUS) at the spleen
or the neck, or the addition of concomitant vagotomy (either at the neck or at
the gastro-esophageal junction [GEJ]). Separate groups of naïve mice
underwent splenic or neck pUS followed by splenectomy for plasma and splenic
molecular analyses.

Charles E.J., Tian Y., Zhang A., Wu D., Mehaffey J.H., Gigliotti J.C., Klibanov A.L., Kron I.L, & Yang Z. (2019). Pulsed Ultrasound Attenuates the Hyperglycemic Exacerbation of Myocardial Ischemia-Reperfusion Injury. The Journal of thoracic and cardiovascular surgery, 161(4), e297-e306.

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