Mots-C Peptide

MOTS-cpeptideyog 16aa peptide encoded los ntawm luv luv qhib nyeem ncej (sORF) nyob rau hauv lub mitochondrial genome 12S rRNA (MT-RNR1), feem ntau sequenced li MRWQEMGYIFYPRKLR. Nws yog nyob rau hauv chav kawm ntawm "mitochondrial-derived peptides" (MDPs).

Nws yog tus cwj pwm los ntawm nws cov keeb kwm hauv mitochondrial DNA, nws thawj txhais lus nyob rau hauv cytoplasm, thiab nws lub luag hauj lwm nyob rau hauv lub systemic signaling, rhuav cov stereotype uas "mtDNA tsuas yog encodes respiratory saw subunits."

Txij li thaum nws cov kev taw qhia txog ib puag ncig xyoo 2015, MOTS-c tau khaws cov pov thawj sai hauv metabolic, kev tawm dag zog lub cev, kev mob thiab kev tiv thaiv kab mob, thiab kev tshawb fawb kev laus, thiab suav tias yog ib qho kev sib txuas hauv mitochondrial -nuclear-systemic metabolic network.

Shaanxi Medibridge muaj kev tshawb fawb-qib MOTS-c ua cov hmoov lyophilized nrog cov ntawv pov thawj purity tsis tsawg dua 99.78%, txhawb nqa los ntawm HPLC thiab pawg-spectrometry QC, batch-to-batch sib xws cov ntaub ntawv, thiab cov ncauj lus kom ntxaws daim ntawv pov thawj ntawm kev soj ntsuam; muab tso rau hauv cov vials tsis muaj menyuam nrog cov pob loj tuaj yeem hloov kho, xa mus rau cov dej khov qhuav, pom zoo cia ntawm −20 degree, rov kho sai hauv cov dej tsis huv lossis tsis muaj, thiab nruj me ntsis rau kev tshawb fawb hauv chav kuaj, tsis yog siv rau kev kuaj mob lossis kev kho mob.

1.High Purity, Identity-Confirmed, Fully Traceable
2. Optimized Stability thiab Formulation rau Cell thiab nyob rau hauv vivo Studies
3. Pov thawj Bioactivity nrog Npaj-to-Siv Method Package
4. Quantification Made Easy: LC–MS/MS thiab Immunoassay Support
5. Sequence Diversity thiab Deep Customization from Mechanism to Translation
6. RUO Kev Ua Raws Cai thiab Tes-On, Kev Pabcuam Txog Kev Tshawb Fawb Txog Kev Tshawb Fawb

1.Biogenesis thiab kev txhais lus Transcribed los ntawm mtDNA (MT-RNR1), tseem muaj pov thawj qhia tias MOTS-c tau txhais feem ntau nyob rau hauv cytosol siv cov noob caj noob ces nuclear-ib qho txawv cross-compartment paradigm (mitochondrial encoding → cytosolic translation).

 

2.State-dependent localization Subcellular distribution is context-driven: chiefly cytosolic at baseline; Nyob rau hauv metabolic los yog oxidative kev nyuaj siab, MOTS-c hloov mus rau lub nucleus thiab pab txhawb rau kev nyuaj siab-adaptive transcriptional programs.

3.Secretion thiab uptake MOTS-c tuaj yeem nkag mus rau hauv cov hlab ntsha raws li cov tshuaj hormones zoo li mitokine los ua kom muaj kev cuam tshuam hauv lub cev. Lub canonical cell-surface receptor tseem raug txhais; uptake yog xav kom koom nrog electrostatic kev sib cuam tshuam thiab endocytic pathways.

Ntawm ib sab MOTS-c peptide primes hlwb kom nkag siab txog lub zog kev ntxhov siab, ua kom AMPK thiab cov phooj ywg-sensing txoj hauv kev. Qhov no hloov cov metabolism mus rau hauv roj-npaum, kev ntxhov siab-hloov hom- txo qis lipogenesis thiab aberrant gluconeogenesis, thaum txhim kho cov piam thaj thiab fatty-acid oxidation. Nyob rau hauv parallel, nws dampens pro-inflammatory tone.

1.Metabolic reprogramming
a.Modulates folate/one-carbon metabolism thiab de novo purine synthesis flux, elevating AICAR (ZMP) kom qhib AMPK.
b.Downstream ntawm AMPK, inhibits mTORC1, txhawb mitochondrial fatty-acid oxidation, nce GLUT4 translocation, thiab suppresses lipogenic signaling (SREBP1c/FASN axis) thiab txawv txav gluconeogenesis.
 

2.Stress → nuclear translocation → transcription
Nyob rau hauv metabolic los yog oxidative kev nyuaj siab, MOTS-c hloov mus rau lub nucleus thiab orchestrates noob cov kev pab cuam txuas rau antioxidant tiv thaiv, metabolic kev nyuaj siab teb, thiab autophagy- txhim kho metabolic yooj thiab ciaj sia taus.
 

3.Inflamation thiab tiv thaiv microenvironment
Tshem tawm cov teeb liab pro-inflammatory (piv txwv li, NF-κB), txo TNF-, IL-6, thiab IL-1; biases macrophage thiab endothelium-lub cev tiv thaiv kab mob mus rau lub xeev anti-inflammatory.

1.In vitro (piv txwv)
a.Skeletal nqaij hlwb: Induce insulin tsis kam nrog palmitate thiab / lossis glucocorticoids; cuam ​​tshuam nrog MOTS-c (nM-μM ntau yam; optimize lub sij hawm-concentration). Kev nyeem ntawv: glucose uptake, GLUT4 translocation, p-AMPK/p-AKT, thiab mitochondrial respiration (Seahorse).
b.Hepatocytes: Thov pub dawb fatty acid (FFA) loading. Cov ntawv nyeem: intracellular triglycerides / lipid droplets, SREBP1c / FASN / CPT1A qhia, mTORC1 kev ua, thiab oxidative-stress indices.
c.Macrophage/Endothelium: Txhawb nrog LPS lossis oxidized LDL. Cov ntawv nyeem: NF-κB nuclear translocation, cytokine profile, nitric oxide (NO) ntau lawm, thiab barrier permeability.

2.In vivo (piv txwv)
a.Metabolic kab mob qauv: HFD/NAFLD; ntsuam xyuas cov tshuaj insulin kam rau siab (ITT), kuaj ntshav qabzib siab (GTT), metabolic cage phenotyping, thiab ua ke cov ntaub so ntswg transcriptomics / metabolomics.
b.Aging/OVX/muscle atrophy qauv: Endpoints muaj xws li cov leeg lub zog / endurance, pob txha ntxhia ceev, inflammatory markers, thiab mitochondrial muaj nuj nqi.

3.Control thiab kev ruaj ntseg zoo
a.Siv equimolar scrambled peptide, cua sov-inactivated tswj, puv koob tshuaj- teb thiab lub sij hawm-course curves, thiab tswj tsheb.
b.Specify peptide purity thiab terminal modifications; txheeb xyuas kev rov ua dua tshiab ntawm cov khoom siv thiab cov khoom muag.
c.Qhov twg ua tau, txhawb kev ua kom muaj txiaj ntsig nrog kev txheeb xyuas cov noob caj noob ces (overexpression/knockdown) lossis txoj hauv kev thaiv (xws li, compound inhibitors/dominant-negative constructs).
 

Thaum GH/IGF-1 workflows, PK/PD cov kev tshawb fawb, thiab cov txheej txheem metabolic xav kom huv, rov tsim cov ntaub ntawv, xaiv Medibridge's high-purity MOTS-c-ua tiav COAs, kev txhawb nqa ceev ceev, thiab kev ntseeg siab los ntawm cov chaw sim thoob ntiaj teb. Rau kev cia siab rau lub sijhawm ntev MOTS-c muab tus khub, email hi@medibridgeapi.com lossis WhatsApp +44 07548632075.

Cim npe nrov: Tuam Tshoj mots-c peptide manufacturers, lwm tus neeg, Hoobkas