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크기 선택
제품정보 (DICE 배송 시 비용 별도)
Linear Formula:
HO2CCH2CH(NH2)CO2H
CAS 번호:
Molecular Weight:
133.10
NACRES:
NA.26
PubChem Substance ID:
eCl@ss:
32160406
UNSPSC Code:
12352209
EC Number:
200-291-6
MDL number:
Beilstein/REAXYS Number:
1723530
제품 이름
L-Aspartic acid, reagent grade, ≥98% (HPLC)
InChI key
CKLJMWTZIZZHCS-REOHCLBHSA-N
InChI
1S/C4H7NO4/c5-2(4(8)9)1-3(6)7/h2H,1,5H2,(H,6,7)(H,8,9)/t2-/m0/s1
SMILES string
N[C@@H](CC(O)=O)C(O)=O
grade
reagent grade
assay
≥98% (HPLC)
form
powder, crystals or chunks
color
white to off-white
mp
>300 °C (dec.) (lit.)
solubility
H2O: 5 mg/mL, 0.5 M HCl: 50 mg/mL (with heat), 1 M NaOH: 50 mg/mL
Quality Level
Gene Information
human ... CA1(759), CA2(760)
rat ... Grin2a(24409)
유사한 제품을 찾으십니까? 방문 제품 비교 안내
Application
L-aspartic acid has been used as one of the components of synthetic drop out media for culturing budding yeast. It has also been used to study non-enzymatic gluconeogenesis.
Biochem/physiol Actions
Aspartic acid is a non-essential amino acid. It is involved in the Urea cycle, Krebs cycle and in DNA metabolism.
Principal neurotransmitter for fast synaptic excitation.
저장 등급
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
dust mask type N95 (US), Eyeshields, Gloves
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The Healing Nutrients Within: Facts, Findings, and New Research on Amino Acids, 1-504 (2007)
Jorge S Valadas et al.
Neuron, 98(6), 1155-1169 (2018-06-12)
Parkinson's disease patients report disturbed sleep patterns long before motor dysfunction. Here, in parkin and pink1 models, we identify circadian rhythm and sleep pattern defects and map these to specific neuropeptidergic neurons in fly models and in hypothalamic neurons differentiated
Nonenzymatic gluconeogenesis-like formation of fructose 1,6-bisphosphate in ice.
Messner CB
Proceedings of the National Academy of Sciences of the USA, 114(28), 7403-7407 (2017)
Eran Mick et al.
eLife, 9 (2020-05-29)
Mitochondrial dysfunction is associated with activation of the integrated stress response (ISR) but the underlying triggers remain unclear. We systematically combined acute mitochondrial inhibitors with genetic tools for compartment-specific NADH oxidation to trace mechanisms linking different forms of mitochondrial dysfunction
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