Results 61 to 70 of about 120,872 (251)

Promyelocytic Leukemia Restricts Enterovirus 71 Replication by Inhibiting Autophagy

open access: yesFrontiers in Immunology, 2018
The promyelocytic leukemia (PML) protein, also known as TRIM19, functions as a major organizer of PML nuclear bodies (NBs) in most mammalian cells and plays important roles in antiviral activities against both DNA and RNA viruses. In this study, we found
Deyan Chen   +8 more
doaj   +1 more source

Brusatol From Suppresses Arsenic Trioxide-Induced PD-L1 Upregulation Through Inhibition of NRF2 in Leukemia Cells

open access: yesNatural Product Communications, 2022
Overexpression of programed death-ligand 1 (PD-L1) is associated with poor prognosis in leukemia. Moreover, antitumor pharmaceuticals have been shown to induce immunoresistance, leading to reduced efficacy.
Shunji Zhang   +3 more
doaj   +1 more source

Targeting CAMKK2 and SOC Channels as a Novel Therapeutic Approach for Sensitizing Acute Promyelocytic Leukemia Cells to All-Trans Retinoic Acid

open access: yesCells, 2021
Calcium ions (Ca2+) play important and diverse roles in the regulation of autophagy, cell death and differentiation. Here, we investigated the impact of Ca2+ in regulating acute promyelocytic leukemia (APL) cell fate in response to the anti-cancer agent ...
Faten Merhi   +9 more
doaj   +1 more source

Expression of the promyelocytic leukemia protein without the nuclear localization signal as a novel diagnostic marker for acute promyelocytic leukemia

open access: yesOncology Reports, 2017
Promyelocytic leukemia-retinoic acid receptor α (PML-RARα) is a fusion protein generated by the t(15;17)(q22;q12) translocation associated with acute promyelocytic leukemia (APL). PML-RARα is cleaved by neutrophil elastase, an early myeloid-specific serine protease, leading to translocation of the nuclear localization signal (NLS) of the PML protein to
Ting, Xu   +6 more
openaire   +3 more sources

A Promyelocytic Leukemia Protein–Thrombospondin-2 Axis and the Risk of Relapse in Neuroblastoma [PDF]

open access: yesClinical Cancer Research, 2016
Abstract Purpose: Neuroblastoma is a childhood malignancy originating from the sympathetic nervous system with a complex biology, prone to metastasize and relapse. High-risk, metastatic cases are explained in part by amplification or mutation of oncogenes, such as MYCN and ALK, and loss of tumor suppressor genes in chromosome band 1p.
Dvorkina, M   +26 more
openaire   +6 more sources

Arsenic sulfide promotes apoptosis in retinoid acid resistant human acute promyelocytic leukemic NB4-R1 cells through downregulation of SET protein. [PDF]

open access: yesPLoS ONE, 2014
Tetra-arsenic tetra-sulfide (As4S4) is an arsenic compound with anti-tumor activity, especially in acute promyelocytic leukemia (APL) that are resistant to retinoic acid (RA).
Yuwang Tian   +10 more
doaj   +1 more source

SUMO pathway dependent recruitment of cellular repressors to herpes simplex virus type 1 genomes [PDF]

open access: yes, 2011
Components of promyelocytic leukaemia (PML) nuclear bodies (ND10) are recruited to sites associated with herpes simplex virus type 1 (HSV-1) genomes soon after they enter the nucleus. This cellular response is linked to intrinsic antiviral resistance and
Delphine Cuchet-Lourenço   +24 more
core   +1 more source

Targeting pseudokinase TRIB3 brings about a new therapeutic option for acute promyelocytic leukemia

open access: yesMolecular & Cellular Oncology, 2017
Pseudokinase tribbles (Trib) family, Trib1 and Trib2, but not Trib3, act as oncogene to drive acute leukemia by destabilizing the myeloid transcription factor CCAAT/enhancer-binding protein α (C/EBPα) and inhibiting myeloid differentiation.
Ke Li, Feng Wang, Zhuo-Wei Hu
doaj   +1 more source

Tumor suppressor function of Gata2 in Acute Promyelocytic Leukemia.

open access: yesBlood, 2021
Most patients with acute promyelocytic leukemia (APL) can be cured with combined All Trans Retinoic Acid (ATRA) and Arsenic Trioxide therapy, which induce the destruction of PML-RARA, the initiating fusion protein for this disease1.
Casey D. S. Katerndahl   +11 more
semanticscholar   +1 more source

Ataxin-1 fusion partners alter polyQ lethality and aggregation [PDF]

open access: yes, 2007
Intranuclear inclusion bodies (IBs) are the histopathologic markers of multiple protein folding diseases. IB formation has been extensively studied using fluorescent fusion products of pathogenic polyglutamine (polyQ) expressing proteins.
Rich, T.   +5 more
core   +1 more source

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