57579
L-胱氨酸 盐酸盐 溶液
10 mM amino acid in 0.1 M HCl, analytical standard
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关于此项目
经验公式（希尔记法）:
C6H12N2O4S2 · HCl
化学文摘社编号:
分子量:
276.76
UNSPSC Code:
85151701
NACRES:
NA.24
PubChem Substance ID:
MDL number:
Beilstein/REAXYS Number:
4828867
产品名称
L-胱氨酸 盐酸盐 溶液, 10 mM amino acid in 0.1 M HCl, analytical standard
InChI
1S/C6H12N2O4S2.ClH/c7-3(5(9)10)1-13-14-2-4(8)6(11)12;/h3-4H,1-2,7-8H2,(H,9,10)(H,11,12);1H/t3-,4-;/m0./s1
SMILES string
Cl.N[C@@H](CSSC[C@H](N)C(O)=O)C(O)=O
InChI key
IOCJWNPYGRVHLN-MMALYQPHSA-N
grade
analytical standard
form
liquid
analyte chemical class(es)
amino acids, peptides, proteins
concentration
10 mM amino acid in 0.1 M HCl
technique(s)
HPLC: suitable
gas chromatography (GC): suitable
color
colorless
application(s)
food and beverages
format
single component solution
storage temp.
2-8°C
Quality Level
Application
有关合适的仪器技术的更多信息，请参阅产品′的检验报告。想要获得更多支持，请联系技术服务部。
signalword
Warning
hcodes
pcodes
Hazard Classifications
Met. Corr. 1
存储类别
8B - Non-combustible corrosive hazardous materials
wgk
nwg
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Faceshields, Gloves, Goggles
Ganeswara Rao Musada et al.
Developmental neurobiology, 80(3-4), 98-110 (2020-04-09)
Muller glia are the predominant glial cell type in the retina, and they structurally and metabolically support retinal neurons. Wnt/β-catenin signaling pathways play essential roles in the central nervous system, including glial and neuronal differentiation, axonal growth, and neuronal regeneration.
Halina T Norbertczak et al.
Tissue engineering. Part C, Methods, 26(11), 565-576 (2020-10-15)
Intervertebral disc (IVD) degeneration is a major cause of back pain. Current surgical interventions have limitations. An alternative approach is to replace degenerated IVDs with a natural biological scaffold. The removal of cellular components from human IVDs should render them
Margaret E Torrence et al.
eLife, 10 (2021-03-02)
The mechanistic target of rapamycin complex 1 (mTORC1) stimulates a coordinated anabolic program in response to growth-promoting signals. Paradoxically, recent studies indicate that mTORC1 can activate the transcription factor ATF4 through mechanisms distinct from its canonical induction by the integrated
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