E3330

E3330 Structure
E3330 structure
Common Name E3330
CAS Number 136164-66-4 Molecular Weight 378.459
Density 1.1±0.1 g/cm3 Boiling Point 542.2±50.0 °C at 760 mmHg
Molecular Formula C21H30O6 Melting Point N/A
MSDS Chinese USA Flash Point 183.2±23.6 °C

Human apurinic/apyrimidinic endonuclease 1 (APE1) has 3' RNA phosphatase and 3' exoribonuclease activities.

J. Mol. Biol. 427(2) , 298-311, (2015)

Apurinic/apyrimidinic endonuclease 1 (APE1) is the predominant mammalian enzyme in DNA base excision repair pathway that cleaves the DNA backbone immediately 5' to abasic sites. In addition to its abasic endonuclease activity, APE1 has 3' phosphatase and 3'-5...

APE1/Ref-1 prevents oxidative inactivation of ERK for G1-to-S progression following lead acetate exposure.

Toxicology 305 , 120-9, (2013)

Apurinic/apyrimidinic endonuclease 1 (APE1)/redox effector factor-1 is a multifunctional enzyme involved in DNA base excision repair and protein redox regulation. Previously, we have showed that lead acetate (Pb) elicits EGFR activation to initiate the SFK/PK...

APE1/Ref-1 regulates STAT3 transcriptional activity and APE1/Ref-1-STAT3 dual-targeting effectively inhibits pancreatic cancer cell survival.

PLoS ONE 7(10) , e47462, (2012)

Pancreatic cancer is a largely incurable disease, and increasing evidence supports strategies targeting multiple molecular mediators of critical functions of pancreatic ductal adenocarcinoma cells. Intracellular redox state modulates the activity of various s...

Soy isoflavones augment radiation effect by inhibiting APE1/Ref-1 DNA repair activity in non-small cell lung cancer.

J. Thorac. Oncol. 6(4) , 688-98, (2011)

Soy isoflavones sensitize cancer cells to radiation both in vitro and in vivo. To improve the effect of radiotherapy for non-small cell lung cancer, we assessed the potential of using a complementary approach with soy isoflavones.Human A549 non-small cell lun...

Characterization of the redox activity and disulfide bond formation in apurinic/apyrimidinic endonuclease.

Biochemistry 51(2) , 695-705, (2012)

Apurinic/apyrimidinic endonuclease (APE1) is an unusual nuclear redox factor in which the redox-active cysteines identified to date, C65 and C93, are surface inaccessible residues whose activities may be influenced by partial unfolding of APE1. To assess the ...

Interactions of apurinic/apyrimidinic endonuclease with a redox inhibitor: evidence for an alternate conformation of the enzyme.

Biochemistry 50(1) , 82-92, (2011)

Apurinic/apyrimidinic endonuclease (APE1) is an essential base excision repair protein that also functions as a reduction and oxidation (redox) factor in mammals. Through a thiol-based mechanism, APE1 reduces a number of important transcription factors, inclu...

NMR studies reveal an unexpected binding site for a redox inhibitor of AP endonuclease 1.

Biochemistry 50(48) , 10540-9, (2011)

AP endonuclease 1 (APE1) is a multifaceted protein with essential roles in DNA repair and transcriptional regulation. APE1 (ref-1) activates many transcription factors (TF), including AP-1 and NF-κB. While the mechanism of APE1 redox activity remains unknown,...

Inhibition of the redox function of APE1/Ref-1 in myeloid leukemia cell lines results in a hypersensitive response to retinoic acid-induced differentiation and apoptosis.

Exp. Hematol. 38(12) , 1178-88, (2010)

The standard of care for promyelocytic leukemia includes use of the differentiating agent all-trans retinoic acid (RA) and chemotherapy. RA induces cell differentiation through retinoic acid receptor (RAR) transcription factors. Because redox mechanisms influ...

Splenectomy enhances liver regeneration through tumor necrosis factor (TNF)-alpha following dimethylnitrosamine-induced cirrhotic rat model.

Hepatogastroenterology. 48(40) , 1022-7, (2001)

We demonstrated that partial splenic embolization for hematological disorders in cirrhotic patients also improved liver function. Therefore, we investigated the mechanism of the beneficial effects of splenectomy on a rat cirrhotic model.1) Rats were administe...

Mad2 haploinsufficiency protects hematopoietic progenitor cells subjected to cell-cycle stress in vivo and to inhibition of redox function of Ape1/Ref-1 in vitro.

Exp. Hematol. 39(4) , 415-23, (2011)

Cell-cycle checkpoints guarantee movement through the cell cycle. Mitotic arrest deficiency 2 (Mad2), a mitotic checkpoint protein, appears crucial for generating the wait anaphase signal to prevent onset of anaphase. We evaluated effects of Mad2 haploinsuffi...