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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

AF4/FMR2 family, member 1

Fel, AF4, MLL/AF4
Top mentioned proteins: MLL, CAN, catalase, HAD, BCR
Papers on Fel
Serial femtosecond crystallography opens new avenues for Structural Biology.
Fromme et al., Tempe, United States. In Protein Pept Lett, Feb 2016
The most successful application of FELs for biology has been the method of serial femtosecond crystallography (SFX) where nano or microcrystals are delivered to the FEL beam in a stream of their mother liquid at room temperature, which ensures the replenishment of the sample before the next X-ray pulse arrives.
Regulation of the imprinted Dlk1-Dio3 locus by allele-specific enhancer activity.
Shilatifard et al., Chicago, United States. In Genes Dev, Feb 2016
Previously, we identified the AF4/FMR2 (AFF) family protein AFF3 within the transcription elongation complex SEC-L3.
MLL-Rearranged Acute Lymphoblastic Leukemias Activate BCL-2 through H3K79 Methylation and Are Sensitive to the BCL-2-Specific Antagonist ABT-199.
Konopleva et al., Houston, United States. In Cell Rep, Jan 2016
The t(4;11) translocation produces an MLL/AF4 fusion protein that activates key target genes through both epigenetic and transcriptional elongation mechanisms.
Multimethod approach for the detection and characterisation of food-grade synthetic amorphous silica nanoparticles.
Barrero-Moreno et al., Italy. In J Chromatogr A, Jan 2016
Dynamic Light Scattering (DLS), Multiangle Light Scattering (MALS), Asymmetric Flow-Field Flow Fractionation (AF4), Inductively Coupled Plasma Mass Spectrometry (ICPMS) and Transmission Electron Microscopy (TEM) were used.
Revisiting the biology of infant t(4;11)/MLL-AF4+ B-cell acute lymphoblastic leukemia.
Menéndez et al., Barcelona, Spain. In Blood, Jan 2016
Among MLL-r infant B-ALL, t(4;11)(+) patients harboring the fusion MLL-AF4 (MA4) display a particularly poor prognosis and a pro-B/mixed phenotype.
[Molecular analysis of childhood B-acute lymphoblastic leukemia: Identification and prognosis of rare breakpoints].
Mehta et al., Delhi, India. In Mol Biol (mosk), Nov 2015
There are four common gene rearrangements which are widely studied to see prognostical values (TEL-AML1, BCR-ABL, E2A-PBX1, MLL-AF4) in childhood B-ALL.
MLL leukemia and future treatment strategies.
Marschalek, Frankfurt am Main, Germany. In Arch Pharm (weinheim), Apr 2015
Except for AF4-MLL, the functional consequences deriving from reciprocal fusion proteins are not very well understood.
[Molecular genetics of acute lymphoblastic leukemia].
Inokuchi et al., Japan. In Rinsho Ketsueki, Mar 2015
Although 5-year overall survival of childhood ALL patients has improved to as much as 90% due to progress in chemotherapy and other supporting therapeutic modalities, including allo-HSCT, the prognosis is still poor for the remaining 10% of cases, which consist mainly of MLL-AF4-positive ALL and bcr-abl positive ALL.
Radiation damage to macromolecules: kill or cure?
Weik et al., Grenoble, France. In J Synchrotron Radiat, Mar 2015
These range over: a proposed new metric derived from atomic B-factors for identifying potentially damaged amino acid residues, a study of the relative damage susceptibility of protein and DNA in a DNA/protein complex, a report of an indication of specific radiation damage to a protein determined from data collected using an X-ray free-electron laser (FEL), an account of the challenges in FEL raw diffraction data analysis, an exploration of the possibilities of using radiation damage induced phasing to solve structures using FELs, simulations of radiation damage as a function of FEL temporal pulse profiles, results on the influence of radiation damage during scanning X-ray diffraction measurements and, lastly, consideration of strategies for minimizing radiation damage during SAXS experiments.
A review of exosome separation techniques and characterization of B16-F10 mouse melanoma exosomes with AF4-UV-MALS-DLS-TEM.
Gale et al., Salt Lake City, United States. In Anal Bioanal Chem, 2014
Exosomes participate in cancer metastasis, but studying them presents unique challenges as a result of their small size and purification difficulties.
Proteasome inhibitors evoke latent tumor suppression programs in pro-B MLL leukemias through MLL-AF4.
Hsieh et al., New York City, United States. In Cancer Cell, 2014
Furthermore, proteasome inhibition conferred preliminary benefit to patients with MLL-AF4 leukemia.
Harnessing the hidden antitumor power of the MLL-AF4 oncogene to fight leukemia.
Hua et al., Philadelphia, United States. In Cancer Cell, 2014
In this issue of Cancer Cell, Liu and colleagues report that a proteasome inhibitor reactivates an MLL-AF4 controlled antitumor program to kill leukemia cells in an oncogene dose- and cell type-dependent manner.
De novo protein crystal structure determination from X-ray free-electron laser data.
Schlichting et al., Heidelberg, Germany. In Nature, 2014
Here we show that X-ray FEL data can be used for de novo protein structure determination, that is, without previous knowledge about the structure.
The mixed lineage leukemia (MLL) fusion-associated gene AF4 promotes CD133 transcription.
Moffat et al., Toronto, Canada. In Cancer Res, 2012
our findings show AF4-dependent regulation of CD133 expression, which is required for the growth of acute lymphoblastic leukemia cells
Lipidic phase membrane protein serial femtosecond crystallography.
Neutze et al., Göteborg, Sweden. In Nat Methods, 2012
X-ray free electron laser (X-FEL)-based serial femtosecond crystallography is an emerging method with potential to rapidly advance the challenging field of membrane protein structural biology.
Methylation-mediated repression of microRNA-143 enhances MLL-AF4 oncogene expression.
Yu et al., Beijing, China. In Oncogene, 2012
miR-143 functions as a tumor suppressor in MLL-AF4 B-cell acute lymphoblastic leukemia.
A genome-wide association study identified AFF1 as a susceptibility locus for systemic lupus eyrthematosus in Japanese.
Yamamoto et al., Yokohama, Japan. In Plos Genet, 2012
we identified a novel association of a variant in the AF4/FMR2 family, member 1 (AFF1) gene at 4q21 with Systemic lupus erythematosus susceptibility (rs340630; P = 8.3x10(-9), odds ratio = 1.21
Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia.
Kouzarides et al., Cambridge, United Kingdom. In Nature, 2011
In vivo studies indicate that I-BET151 has significant therapeutic value, providing survival benefit in two distinct mouse models of murine MLL-AF9 and human MLL-AF4 leukaemia.
Insights into the cellular origin and etiology of the infant pro-B acute lymphoblastic leukemia with MLL-AF4 rearrangement.
Menendez et al., Granada, Spain. In Leukemia, 2011
MLL-AF4 leukemogenesis has been particularly difficult to model and bona fide MLL-AF4 disease models do not exist so far.[review]
The leukemogenic AF4-MLL fusion protein causes P-TEFb kinase activation and altered epigenetic signatures.
Marschalek et al., Frankfurt am Main, Germany. In Leukemia, 2011
findings suggest that the AF4-MLL protein disturbs the fine-tuned activation cycle of promoter-arrested RNA Pol II and causes altered histone methylation signatures
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