SML1735
PFM01
≥98% (HPLC)
동의어(들):
(5Z)-5-[(4-Hydroxyphenyl)methylene]-3-(2-methylpropyl)-2-thioxo-4-thiazolidinone, 5-(4-Hydroxybenzylidene)-3-isobutyl-2-thioxothiazolidin-4-one
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모든 사진(1)
About This Item
실험식(Hill 표기법):
C14H15NO2S2
CAS Number:
Molecular Weight:
293.40
MDL number:
UNSPSC 코드:
12352200
PubChem Substance ID:
NACRES:
NA.77
추천 제품
Quality Level
분석
≥98% (HPLC)
양식
powder
색상
white to beige
solubility
DMSO: 20 mg/mL, clear
저장 온도
2-8°C
SMILES string
OC1=CC=C(/C=C2SC(N(CC(C)C)C\2=O)=S)C=C1
InChI
1S/C14H15NO2S2/c1-9(2)8-15-13(17)12(19-14(15)18)7-10-3-5-11(16)6-4-10/h3-7,9,16H,8H2,1-2H3/b12-7-
InChI key
GPURHDUTZUYAFI-GHXNOFRVSA-N
생화학적/생리학적 작용
PFM01 is a cell-permeable N-alkylated Mirin (Sigma Cat. No. 475954) derivative that selectively inhibits against MRE11 endo-, but not exo-, nuclease activity. PFM01 targets MRE11 at a site near the dimer interface, distinct from that occupied by Mirin and PFM39 to allow disruption of the ssDNA-binding groove and selective inhibition against MRE11 endo-, but not exo-, nuclease activity. While both endonuclease and exonuclease activities are required for MRE11-mediated homologous recombination (HR) repair, only FM01 (100 μM), but not the exonuclease inhibitors Mirin (500 μM) and PFM39 (100 μM), rescues G2-phase double-strand break (DSB) repair defect in HR protein BRCA2-deficient HSC62-hTERT fibroblasts following ionizing irradiation (IR) by blocking HR initiation and thereby allowing non-homologous end joining (NHEJ) to proceed.
PFM01 is a cell-permeable N-alkylated Mirin derivative that selectively inhibits against MRE11 endo-, but not exo-, nuclease activity.
신호어
Warning
유해 및 위험 성명서
Hazard Classifications
Acute Tox. 4 Oral - Eye Irrit. 2 - Skin Irrit. 2
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
가장 최신 버전 중 하나를 선택하세요:
Donna R Whelan et al.
Proceedings of the National Academy of Sciences of the United States of America, 118(11) (2021-03-13)
Homologous recombination (HR) is a major pathway for repair of DNA double-strand breaks (DSBs). The initial step that drives the HR process is resection of DNA at the DSB, during which a multitude of nucleases, mediators, and signaling proteins accumulates
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