Neuromedin N
(Synonyms: Neuromedin N (rat, mouse, porcine, canine)) 目录号 : GC36726
A neurotensin-like neuropeptide
Cas No.:92169-45-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Neuromedin N is a neurotensin-like hexapeptide that is synthesized from the same precursor as neurotensin.1 It is highly expressed in the brain but is also expressed in the gastrointestinal system and adrenal glands. It competitively inhibits neurotensin binding to rat brain synaptic membranes and has increased potency in the presence of the peptidase inhibitor bestatin (IC50s = 16.7 and 3 nM, respectively).2 Neuromedin N (10 pM) increases the phagocytic function of isolated murine peritoneal macrophages and increases chemotaxis two-fold compared with control, an effect that is blocked by the calcium-channel blocker ryanodine.3 It induces hypotension in rats and contraction of isolated guinea pig ileum.4 Neuromedin N (0.05 - 5 μg, i.c.v.) also elicits hypothermia in rats in a dose- and time-dependent manner, which is potentiated by bestatin .5 Neuromedin N is more potent than neurotensin in stimulating spontaneous motor activity and increasing dopamine metabolism in several brain regions following injection into the rat ventral tegmental area but is less potent than neurotensin when injected into the nucleus accumbens.6
1.Kitabgi, P.Neurotensin and neuromedin N are differentially processed from a common precursor by prohormone convertases in tissues and cell linesResults Probl. Cell Differ.5085-96(2010) 2.Checler, F., Vincent, J.P., and Kitabgi, P.Neuromedin N: High affinity interaction with brain neurotensin receptors and rapid inactivation by brain synaptic peptidasesEur. J. Pharmacol.126(3)239-244(1986) 3.De la Fuente, M., Garrido, J.J., Arahuetes, R.M., et al.Stimulation of phagocytic function in mouse macrophages by neurotensin and neuromedin NJ. Neuroimmunol.42(1)97-104(1993) 4.Minamino, N., Kangawa, K., and Matsuo, H.Neuromedin N: A novel neurotensin-like peptide identified in porcine spinal cordBiochem. Biophys. Res. Commun.122(2)542-549(1984) 5.Dubuc, I., Nouel, D., Coquerel, A., et al.Hypothermic effect of neuromedin N in mice and its potentiation by peptidase inhibitorsEur. J. Pharmacol.151(1)117-121(1988) 6.Kalivas, P.W., Richardson-Carlson, R., and Duffy, P.Neuromedin N mimics the actions of neurotensin in the ventral tegmental area but not in the nucleus accumbensJ. Pharmacol. Exp. Ther.238(3)1126-1131(1986)
| Cas No. | 92169-45-4 | SDF | |
| 别名 | Neuromedin N (rat, mouse, porcine, canine) | ||
| 分子式 | C38H63N7O8 | 分子量 | 745.95 |
| 溶解度 | Water: 50 mg/mL (67.03 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.3406 mL | 6.7029 mL | 13.4057 mL |
| 5 mM | 0.2681 mL | 1.3406 mL | 2.6811 mL |
| 10 mM | 0.1341 mL | 0.6703 mL | 1.3406 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Pro-neurotensin/Neuromedin N and Hypertension Risk: A Prospective Study
Am J Hypertens 2022 Mar 8;35(3):281-288.PMID:34655288DOI:10.1093/ajh/hpab166.
Background: Neurotensin, a neuropeptide with direct cardiac effects, has been associated with prospective risk of hypertension-related conditions through measurement of its precursor, pro-neurotensin/Neuromedin N (pro-NT/NMN). Its association with incident hypertension has not been evaluated. Methods: From 2003 to 2007, the REasons for Geographic And Racial Differences in Stroke (REGARDS) study enrolled 30,239 Black or White adults age ≥45. Pro-NT/NMN was measured in 1,692 participants without baseline hypertension (self-reported antihypertensive use or blood pressure ≥140/90 mm Hg) who underwent follow-up assessment in 2013-2016. A sensitivity analysis was conducted using a lower threshold (≥130/80 mm Hg) to define hypertension. Three robust Poisson regression models were fitted to risk of incident hypertension, adding demographics, cardiometabolic risk factors, and dietary covariates. Results: Six hundred and fourteen participants developed hypertension over 9.4 years of follow-up. Pro-NT/NMN ranged from 14 to 1,246 pmol/l, with median [interquartile range] 154 [112, 206] pmol/l. Pro-NT/NMN was not associated with hypertension overall (fully adjusted incidence rate ratio per SD increment log pro-NT/NMN 1.03, 95% confidence interval 0.95-1.11). Results of sensitivity analysis did not differ substantially. Conclusions: Baseline pro-NT/NMN was not associated with incident hypertension. This may be a result of neurotensin's long-term interactions with other molecular regulators of blood pressure, such as the renin-angiotensin-aldosterone system.
Neurotensin and Neuromedin N are differentially processed from a common precursor by prohormone convertases in tissues and cell lines
Results Probl Cell Differ 2010;50:85-96.PMID:19862492DOI:10.1007/400_2009_27.
Neurotensin (NT) is synthesized as part of a larger precursor that also contains Neuromedin N (NN), a six amino acid NT-like peptide. NT and NN are located in the C-terminal region of the precursor (pro-NT/NN) where they are flanked and separated by three Lys-Arg sequences. A fourth dibasic sequence is present in the middle of the precursor. Dibasics are the consensus sites recognized and cleaved by specialized endoproteases that belong to the family of proprotein convertases (PCs). In tissues that express pro-NT/NN, the three C-terminal Lys-Arg sites are differentially processed, whereas the middle dibasic is poorly cleaved. Processing gives rise mainly to NT and NN in the brain, NT and a large peptide with a C-terminal NN moiety (large NN) in the gut, and NT, large NN, and a large peptide with a C-terminal NT moiety (large NT) in the adrenals. Recent evidence indicates that PC1, PC2, and PC5-A are the prohormone convertases responsible for the processing patterns observed in the gut, brain, and adrenals, respectively. As NT, NN, large NT, and large NN are all endowed with biological activity, the evidence reviewed here supports the idea that posttranslational processing of pro-NT/NN in tissues may generate biological diversity of pathophysiological relevance.
Inactivation of neurotensin and Neuromedin N by Zn metallopeptidases
Peptides 2006 Oct;27(10):2515-22.PMID:16904239DOI:10.1016/j.peptides.2005.12.017.
The two related peptides neurotensin (NT) and Neuromedin N (NN) are efficiently inactivated by peptidases in vitro. Whereas NT is primarily degraded by a combination of three Zn metallo-endopeptidases, namely endopeptidases 24.11, 24.15 and 24.16, in all systems examined, NN is essentially inactivated by the Zn metallo-exopeptidase aminopeptidase M. In this paper we review the work that has led to the identification of the NT- and NN-degrading enzymes and to the purification and cloning of EP 24.16, a previously unidentified peptidase. We provide a brief description of the three NT-inactivating endopeptidases and of their specific and mixed inhibitors, some of them developed in the course of studying NT degradation. Finally, we review in vivo data obtained with these inhibitors that strongly support a physiological role for EP 24.11, 24.15 and 24.16 in the termination of NT-generated signals and for aminopeptidase in terminating NN action. Knowledge of the NT and NN inactivation mechanisms offers the perspective to develop metabolically stable analogs of these peptides with potential therapeutic value.
Pro-Neurotensin/Neuromedin N and Risk of Cognitive Impairment in a Prospective Study
J Alzheimers Dis 2020;76(4):1403-1412.PMID:32623400DOI:10.3233/JAD-200456.
Background: The neuropeptide neurotensin (NT) has been linked to cardiometabolic disease. Cardiovascular risk factors are being recognized as risk factors for cognitive impairment. Objective: To examine the association of the stable precursor of NT, pro-neurotensin/Neuromedin N (pro-NT/NMN), with incident cognitive impairment (ICI). Methods: We conducted a prospective nested case-control study in the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort. In 2003-2007, REGARDS enrolled 30,239 Black and White adults aged ≥45 years. ICI was identified using a 3-test cognitive battery administered biannually. Baseline pro-NT/NMN was measured by immunoassay in 393 cases of ICI and 490 controls after 3.4 years follow up. Multivariable logistic regression was used to calculate odds ratios (OR) of ICI by pro-NT/NMN quartiles. Race, age, and sex differences were studied with stratified models and interaction testing. Results: Pro-NT/NMN was higher in Black participants and those with hypertension and diabetes. Women with a 4th versus 1st-quartile pro-NT/NMN had 2.28-fold increased odds of ICI (95% CI 1.08-4.78) after adjusting for risk factors and incident stroke. There was no association of higher pro-NT/NMN quartiles with ICI in the overall group or men. There were no race or age differences in associations. Conclusion: In this biracial population-based study, elevated systemic pro-NT/NMN was associated with more than doubled risk of ICI in women but not men. Others reported sex-specific associations in women for cardiovascular mortality and diabetes with higher pro-NT/NMN, supporting a role for future research on sex differences in the neurotensinergic system.
Differential processing of pro-neurotensin/Neuromedin N and relationship to pro-hormone convertases
Peptides 2006 Oct;27(10):2508-14.PMID:16904237DOI:10.1016/j.peptides.2006.03.038.
Neurotensin (NT) is synthesized as part of a larger precursor that also contains Neuromedin N (NN), a six amino acid neurotensin-like peptide. NT and NN are located in the C-terminal region of the precursor (pro-NT/NN) where they are flanked and separated by three Lys-Arg sequences. A fourth dibasic sequence is present in the middle of the precursor. Dibasics are the consensus sites recognized and cleaved by endoproteases that belong to the recently identified family of pro-protein convertases (PCs). In tissues that express pro-NT/NN, the three C-terminal Lys-Arg sites are differentially processed, whereas the middle dibasic is poorly cleaved. Pro-NT/NN processing gives rise mainly to NT and NN in the brain, to NT and a large peptide ending with the NN sequence at its C-terminus (large NN) in the gut and to NT, large NN and a large peptide ending with the NT sequence (large NT) in the adrenals. Recent evidence indicates that PC1, PC2 and PC5-A are the pro-hormone convertases responsible for the processing patterns observed in the gut, brain and adrenals, respectively. As NT, NN, large NT and large NN are all endowed with biological activity, the evidence reviewed here supports the idea that post-translational processing of pro-NT/NN in tissues may generate biological diversity.