Siagoside
Siagoside is an inner ester of Ganglioside GM1 (HY-N10546). Siagoside selectively attenuates morphological and functional striatal impairments induced by transient forebrain ischemia in rats. Siagoside can be used for the research of neurological disease, such as acute cerebral ischemia.
연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.
- CAS No.: 100345-64-0
- 화학식: C73H129N3O30
- 분자량:1528.81
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
Chemical Information
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CAS No. 100345-64-0
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분자량 1528.81
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화학식 C73H129N3O30
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SMILES
O=C(C)NC1C(CC2(OC3C(C(OC4C(C(C(OC4CO)OCC(C(/C=C/CCCCCCCCCCCCC)O)NC(CCCCCCCCCCCCCCCCC)=O)O)O)OC(C3OC5OC(C(C(C5NC(C)=O)OC6OC(C(C(C6O)O)O)CO)O)CO)CO)OC2=O)OC1C(C(CO)O)O)O
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)