2. Apoptosis Membrane Transporter/Ion Channel Epigenetics PI3K/Akt/mTOR
  3. Apoptosis GLUT AMPK
  4. MOTS-c (human)

MOTS-c (human) 是一种可穿透血脑屏障的、线粒体来源的多肽，调节 AMPK/PGC-1α 通路增强胰岛素敏感性。MOTS-c (human) 抑制叶酸循环和嘌呤从头合成，升高 AICAR 水平以激活 AMPK，进而调控 Nrf2/Keap1 抗氧化通路及抑制NF-κB炎症通路，同时促进线粒体生物发生和能量代谢。MOTS-c (human) 具有改善糖脂代谢、抗氧化应激、抗炎及神经保护的作用，可用于 2 型糖尿病、创伤性脑损伤、炎症性疾病及衰老相关代谢紊乱等研究。 (高分辨率测序的最新进展导致发现了源自线粒体基因组的独特肽。目前已鉴定出 8 种肽：护脑素、12S tRNA-c (MOTS-c) 的线粒体开放阅读框和 6 种小肽 (护脑素样肽 (SHLP1-6))。所有这些肽均从线粒体释放到细胞质中，并与延长寿命和细胞活力、减少细胞凋亡和其他有益功能相关。

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Custom Peptide Synthesis

MOTS-c (human)

MOTS-c (human) Chemical Structure

CAS No. : 1627580-64-6

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Other Forms of MOTS-c (human):

MOTS-c (human) 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

MOTS-c (human) is a blood-brain barrier-penetrating, mitochondrial-derived peptide that modulates the AMPK/PGC-1α pathway to enhance insulin sensitivity. MOTS-c (human) inhibits the folate cycle and de novo purine synthesis, increases AICAR levels to activate AMPK, and then regulates the Nrf2/Keap1 antioxidant pathway and inhibits the NF-κB inflammatory pathway, while promoting mitochondrial biogenesis and energy metabolism. MOTS-c (human) has the effects of improving glucose and lipid metabolism, anti-oxidative stress, anti-inflammatory and neuroprotection, and can be used in the study of type 2 diabetes, traumatic brain injury, inflammatory diseases and aging-related metabolic disorders[1][2][3][4].

IC50 & Target

GLUT4

 

AMPK

 

AICAR

 

体外研究
(In Vitro)

基于高分辨率测序技术的应用，促成了源自线粒体基因组的独特肽的发现。目前已鉴定出八种肽：人源肽、12S tRNA-c 的线粒体开放阅读框 (MOTS-c) 以及六种短肽 (人源肽样肽 (SHLP1-6))。所有这些肽均从线粒体释放到细胞质中，并与延长寿命和细胞活力、减少细胞凋亡以及其他有益功能相关[1]。
MOTS-c (human) (10 μM；24-72 h) 在 HEK293 细胞中激活 AMPK (Thr172 磷酸化) 及下游抗氧化蛋白 Nrf2、Keap1 表达，并抑制 MAPKs (ERK、JNK、P38) 磷酸化[2]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

MOTS-c (human) 相关抗体:

Western Blot Analysis[2]

Cell Line: HEK293 cells
Concentration: 10 μM
Incubation Time: 24-72 h
Result: Significantly increased phosphorylation of AMPK at Thr172 and protein levels of Nrf2 and Keap1, while reducing phosphorylation of ERK, JNK, and P38.
Resulted activation of AMPK by densitometric quantification, with a 2-fold increase in p-AMPK/AMPK ratio compared to control.
Attenuated these effects by co-treatment with the AMPK inhibitor.
体内研究
(In Vivo)

MOTS-c (human) (25-50 mg/kg；腹腔注射；每日 1 次；21 天) 在雄性 C57BL/6 小鼠的创伤性脑损伤模型中，可减轻神经功能缺损，抑制脑组织 HMGB1/TLR4/NF-κB 炎症通路[2]。
MOTS-c (human) (5 mg/kg；腹腔注射；每日 2 次；4 天) 在雄性 CD-1 小鼠的急性处理模型中，可通过招募 IL-6 和 TNF-α，减轻与肥胖和胰岛素抵抗相关炎症[2]。
MOTS-c (human) (50 mg/kg；腹腔注射；每日 1 次；单次给药) 在雄性 ICR 小鼠的福尔马林炎症模型中，可减少舔爪时间，抑制脊髓 p-ERK/p-JNK/p-P38 及 c-fos 表达，发挥抗伤害性和抗炎作用[3]。
MOTS-c (human) (0.5 mg/kg；腹腔注射；每日 1 次；8 周) 在雄性 Sprague-Dawley 大鼠 2 型糖尿病模型中，可降低空腹血糖、糖化血清蛋白及血脂水平，改善心肌超微结构损伤并激活心肌 AMPK/Nrf2 抗氧化通路[4]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male C57BL/6 mice (6-8-week-old) with controlled-cortical impact (CCI)-induced traumatic brain injury model[2]
Dosage: 25 mg/kg, 50 mg/kg (saline)
Administration: Intraperitoneal injection, once daily, for 21 days starting 1 hour post-injury
Result: At 50 mg/kg, MOTS-c reduced neurological severity scores (NSS) by 45% and improved rotarod performance (latency increased by 50%) compared to injured controls.
Brain tissue analysis showed reduced HMGB1 expression (30% decrease), TLR4/NF-κB pathway inhibition, and lower pro-inflammatory cytokines (TNF-α, IL-6) in the ipsilateral cortex.
OBB-NC formulation (3 mg/kg) showed comparable effects with enhanced BBB penetration.
Animal Model: Male ICR mice (25-30 g, 6-week-old) with Formalin-induced paw inflammation model[3]
Dosage: 50 mg/kg (saline)
Administration: Intraperitoneal injection, 1 hour before formalin challenge, single dose
Result: Significantly reduced licking time in the late phase (phase II, 11-40 min) by 60% compared to vehicle controls.
Immunohistochemistry revealed decreased c-fos positive cells (40% reduction) in the spinal dorsal horn, with Western blot confirming suppressed phosphorylation of ERK (Thr202/Tyr204), JNK (Thr183/Tyr185), and P38 (Thr180/Tyr182) by 30-50%.
The AMPK inhibitor Compound C abolished these effects.
Animal Model: Male Sprague-Dawley rats (220-240 g, 7-week-old) with high-fat diet/streptozotocin-induced type 2 diabetes model[4]
Dosage: 0.5 mg/kg (saline)
Administration: Intraperitoneal injection, once daily, for 8 weeks
Result: Significantly decreased fasting blood glucose (FBG) by 35%, HOMA-IR by 40%, and plasma triglycerides (TG)/total cholesterol (TC) by 25-30% compared to diabetic controls.
Reduced mitochondrial swelling and cristae damage, with increased SOD/GSH activity and upregulated p-AMPK, Nrf2, and Keap1 protein expression in the heart.
Combined with exercise, MOTS-c further enhanced glucose disposal and attenuated oxidative stress (MDA reduction by 50%).
分子量

2174.59

Formula

C101H152N28O22S2
CAS 号
性状

固体

颜色

White to off-white

Sequence

Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg
Sequence Shortening

MRWQEMGYIFYPRKLR
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Sealed storage, away from moisture

Powder -80°C 2 years
-20°C 1 year

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

纯度 & 产品资料

纯度: 99.90%

COA (286 KB) RP-HPLC (109 KB) MS (240 KB) 元素分析报告 (210 KB)

产品使用指南 (1538 KB)
参考文献

MOTS-c (human) 相关分类

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  • 稀释计算器

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

MOTS-c (human)1627580-64-6ApoptosisGLUTAMPKGlucose transporter AMP-activated protein kinaseInhibitorinhibitorinhibit

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