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Merck
모든 사진(1)

주요 문서

SML1169

Sigma-Aldrich

Pitstop 2

≥98% (HPLC), powder, clathrin-mediated endocytosis inhibitor

동의어(들):

N-[5-[(4-Bromophenyl)methylene]-4,5-dihydro-4-oxo-2-thiazolyl]-1-naphthalenesulfonamide, Pitstop-2

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About This Item

실험식(Hill 표기법):
C20H13BrN2O3S2
CAS Number:
Molecular Weight:
473.36
UNSPSC 코드:
12352200
NACRES:
NA.77

제품명

Pitstop 2, ≥98% (HPLC)

Quality Level

분석

≥98% (HPLC)

양식

powder

색상

white to light brown

solubility

DMSO: 20 mg/mL, clear

저장 온도

−20°C

애플리케이션

Pitstop 2 has been used as an inhibitor of clathrin-mediated endocytosis.

생화학적/생리학적 작용

Pitstop 2 also has an ability to breakdown the nuclear pore complex (NPC) permeability barrier and decrease importin β binding along with alteration of the NPC ultrastructure. Pitstop 2 is also involved in the inhibition of platelet activation, platelet aggregation and secretion.
Pitstop 2 is a selective inhibitor of clathrin-mediated endocytosis that acts via blocking ligand access to the clathrin terminal domain. Pitstop 2 selectively inhibits clathrin-mediated HIV entry and stalls clathrin-coated pit (CCP) dynamics.
Pitstop 2 is a selective inhibitor of clathrin-mediated endocytosis.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


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Journal of proteomics, 227, 103918-103918 (2020-07-28)
Bacterial insecticidal proteins, such as the Bin toxin from Lysinibacillus sphaericus, could be used more extensively to control insecticide resistant mosquitoes. This study was aimed at identification of mosquito cell proteins binding Bin toxin. Results showed that purified toxin was
Clathrin inhibitor Pitstop-2 disrupts the nuclear pore complex permeability barrier
Liashkovich I, et al.
Scientific Reports, 5, 9994-9994 (2015)
Clathrin-mediated integrin ?IIb?3 trafficking controls platelet spreading
Gao W, et al.
Platelets, 1-12 (2017)
Maria S Ioannou et al.
Cell, 177(6), 1522-1535 (2019-05-28)
Metabolic coordination between neurons and astrocytes is critical for the health of the brain. However, neuron-astrocyte coupling of lipid metabolism, particularly in response to neural activity, remains largely uncharacterized. Here, we demonstrate that toxic fatty acids (FAs) produced in hyperactive

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