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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크기 선택
제품정보 (DICE 배송 시 비용 별도)
실험식(Hill 표기법):
C14H15NO2S2
CAS 번호:
Molecular Weight:
293.40
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
제품 이름
PFM01, ≥98% (HPLC)
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
SMILES string
OC1=CC=C(/C=C2SC(N(CC(C)C)C\2=O)=S)C=C1
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 20 mg/mL, clear
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
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.
signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral - Eye Irrit. 2 - Skin Irrit. 2
저장 등급
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Lea Völkening et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(2), 2812-2820 (2020-01-08)
The Mre11A/RAD50/NBN complex (MRN) is an essential regulator of the cellular damage response after DNA double-strand breaks (DSBs). More recent work has indicated that MRN may also impact on the duration of mitosis. We show here that RAD50-deficient fibroblasts exhibit
Sarah R Hengel et al.
Cell chemical biology, 24(9), 1101-1119 (2017-09-25)
To maintain stable genomes and to avoid cancer and aging, cells need to repair a multitude of deleterious DNA lesions, which arise constantly in every cell. Processes that support genome integrity in normal cells, however, allow cancer cells to develop
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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