推荐产品
产品名称
L-苏氨酸, reagent grade, ≥98% (HPLC)
等级
reagent grade
质量水平
方案
≥98% (HPLC)
表单
powder
颜色
white to off-white
mp
256 °C (dec.) (lit.)
溶解性
H2O: 50 mg/mL, clear, colorless
应用
cell analysis
SMILES字符串
C[C@@H](O)[C@H](N)C(O)=O
InChI
1S/C4H9NO3/c1-2(6)3(5)4(7)8/h2-3,6H,5H2,1H3,(H,7,8)/t2-,3+/m1/s1
InChI key
AYFVYJQAPQTCCC-GBXIJSLDSA-N
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应用
L-苏氨酸已被用于转化后细胞的选择。其已被用于研究氨基酸在促进果蝇（Drosophila melanogaster）食物消耗中的作用。
生化/生理作用
L-苏氨酸是一种必需氨基酸。它可参与粘蛋白的合成，粘蛋白是一种支持肠功能和完整性的蛋白质。L-苏氨酸在免疫系统、O-连接糖基化、蛋白质磷酸化和甘氨酸合成中发挥作用。
储存分类代码
11 - Combustible Solids
WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, type N95 (US)
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
Markerless Gene Editing in the Hyperthermophilic Archaeon Thermococcus kodakarensis
Alexandra M. Gehring
Bio-protocol, 7(22), 1-26 (2017)
An internal sensor detects dietary amino acids and promotes food consumption in Drosophila
Zhe Yang
Nature, 1-36 (2017)
Yongxian Zhuang et al.
PloS one, 9(9), e108444-e108444 (2014-09-26)
Different cancer cells exhibit altered sensitivity to metformin treatment. Recent studies suggest these findings may be due in part to the common cell culture practice of utilizing high glucose, and when glucose is lowered, metformin becomes increasingly cytotoxic to cancer
Voltage-Gated Proton Channels as Novel Drug Targets: From NADPH Oxidase Regulation to Sperm Biology.
Tamara Seredenina et al.
Antioxidants & redox signaling, 23(5), 490-513 (2014-02-04)
Voltage-gated proton channels are increasingly implicated in cellular proton homeostasis. Proton currents were originally identified in snail neurons less than 40 years ago, and subsequently shown to play an important auxiliary role in the functioning of reactive oxygen species (ROS)-generating
Mario Ost et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 29(4), 1314-1328 (2014-12-11)
Recent studies on mouse and human skeletal muscle (SM) demonstrated the important link between mitochondrial function and the cellular metabolic adaptation. To identify key compensatory molecular mechanisms in response to chronic mitochondrial distress, we analyzed mice with ectopic SM respiratory
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