The role of PML in tumor suppression.

By P. Salomoni, P. Pandolfi. Cell, 2002

603 citations recorded by the source corpus.

Subfields: Biochemistry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/072e460e9fd4210906b9ca6fcd618898174a0c3c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biochemistry

D. Cobrinik

In Molecular Biology

Citations in the corpus

Structure, dynamics and functions of promyelocytic leukaemia nuclear bodies (2007, background): “, are now simply called PML-nuclear bodies (PML-NBs) because the Pml gene is essential for their formatio”
Apoptosis and Molecular Targeting Therapy in Cancer (2014, background): “Several proteins that can promote apoptosis have been localized to PODs, including Daax, Zip kinase, and Par4, and defects in assembly of these nuclear structures are documented in cancers [25].”
Arsenic degrades PML or PML–RARα through a SUMO-triggered RNF4/ubiquitin-mediated pathway (2008, background): “They depend on PML for their organization and have been implicated in the regulation of many processe”
Pocket proteins and cell cycle control (2005, background): “…induce the formation of PML nuclear bodies (Fang et al., 2002), which have widespread effects on cell proliferation, differentiation, and survival (Salomoni and Pandolfi, 2002). pRB can also suppress Ras signaling (Lee et al., 1999) and augment expression of differentiation-associated genes…”
TRIM/RBCC, a novel class of ‘single protein RING finger’ E3 ubiquitin ligases (2005, background): “1 trancriptional activity (91) TRIM16/EBBP Regulation of keratinocyte differentiation (92) TRIM18/MID1 Regulation of microtubule dynamics X-linked Opitz syndrome (23,64) TRIM19/PML Apoptosis/Senescence/Restriction to viral infection Tumor suppressor (49,86) TRIM20/Pyrin/Marenostrin Apoptosis Familia”
Phosphorylation of BLM, Dissociation from Topoisomerase IIIα, and Colocalization with γ-H2AX after Topoisomerase I-Induced Replication Damage (2005, background): “The PML gene, originally identified as the translocation site with the retinoic acid receptor- (RAR ) gene forms the PML-RAR fusion protein in promyelocytic leukemia (8, 16, 56, 57).”