Description
Pyr41 (418805-02-4) inhibits ubiquitin activating enzyme E1 (>60% inhibition at 10 μM) with little or no activity against E2 or E3. Cell permeable
Uses
PYR 41 is an irreversible and cell-permeable UBE1 inhibitor.
Definition
ChEBI: PYR-41 is an ethyl ester resulting from the formal condensation of the carboxy group of 4-{4-[(5-nitrofuran-2-yl)methylidene]-3,5-dioxopyrazolidin-1-yl}benzoic acid with ethanol. It is an irreversible and cell-permeable inhibitor of ubiquitin-activating enzyme E1. It has a role as an EC 6.2.1.45 (E1 ubiquitin-activating enzyme) inhibitor and an antineoplastic agent. It is an ethyl ester, a member of furans, a C-nitro compound, a member of pyrazolidines and a benzoate ester.
Biochem/physiol Actions
PYR-41 is a cell permeable inhibitor of Ubiquitin activating enzyme (E1) with little or no activity against E3, E2, or caspase enzymatic activity.
in vitro
in addition to blocking ubiquitylation, pyr-41 was found to increase total sumoylation in cells. pyr-41 could attenuate cytokine-mediated nuclear factor-kbactivation. this correlated with inhibition of nonproteasomal ubiquitylation of traf6, which is important to ikbkinase activation. pyr-41 also prevented the downstream ubiquitylation and proteasomal degradation of ikba. moreover, pyr-41 has demonstrated effective uae e1 inhibition as well as some off-target inhibition of the other ubiquitin regulatory enzymes and signal-transducing proteins, suggesting it is a nonspecific inhibitor [1].
Enzyme inhibitor
This cell-permeable pyrazone (FW = 425.40 g/mol; CAS 418805-02-4),
also known as 4- (4- (5-nitrofuran-2-ylmethylene) -3,5-dioxo-pyrazolidin-1-
yl) benzoic acid ethyl ester, irreversibly inhibits the ubiquitin-activating
enzyme E1 activity (IC50 <10 μM in cell-free E1 ubiquitination assays) but
exhibits little or no activity against E3, E2, or caspase enzymatic activity.
PYR-41 blocks ubiquitination-dependent protein degradation and other
ubiquitination-mediated cellular activities. Unexpectedly, in addition to
blocking ubiquitylation, PYR-41 increases total sumoylation in cells.
Although the molecular basis for this effect is unknown, increased
sumoylation is also observed in cells harboring a temperature-sensitive form
of E1. PYR-41 attenuates cytokine-mediated NFkb activation. This behavior
correlates with inhibition of nonproteasomal (Lys-63) ubiquitylation of
TRAF6, a protein that is essential to Ikb kinase activation. PYR-41 also
prevents the downstream ubiquitylation and proteasomal degradation of
Ikb. (See also NSC624206) Later studies demonstrated not only PYR-41
inhibited UBE1 but also had equal or greater inhibitory activity against
several deubiquitinases (DUBs) within intact cells and purified Ubiquitin-
Specific Peptidase 5 (USP5) in vitro. Both UBE1 and DUB inhibition
are mediated through covalent protein cross-linking, which parallels the
inhibition of the target proteins enzymatic activity. PYR-41 also mediates
cross-linking of specific protein kinases (Bcr-Abl, Jak2) to inhibit their
signaling activity. Degradation of Repressor Element 1-Silencing
transcription factor (REST), itself is a major neuronal and tumor suppressor,
is blocked by both PYR-41 and the proteasome inhibitor MG-132, but not
by the nuclear export inhibitor leptomycin B.
References
1) Yang et al. (2007), Inhibitors of Ubiquitin-Activating Enzyme (E1), a New Class of Potential Cancer Therapeutics; Cancer Res., 67 9472
2) Mi et al. (2009), Cancer Preventive isothiocyanates induce selective degradation of cellular alpha- and beta-tubulins by proteasomes; J. Biol. Chem., 284 17039
3) Maehama et al. (2014), Nucleolar Stress Induces Ubiquitination-independent Proteasomal Degradation of PICT1 Protein PYR41; J. Biol. Chem., 289 20802 [Focus Citation]