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Nucleoporin 98kDa

NUP98, Nup96
Signal-mediated nuclear import and export proceed through the nuclear pore complex (NPC), which is comprised of approximately 50 unique proteins collectively known as nucleoporins. The 98 kDa nucleoporin is generated through a biogenesis pathway that involves synthesis and proteolytic cleavage of a 186 kDa precursor protein. This cleavage results in the 98 kDa nucleoporin as well as a 96 kDa nucleoporin, both of which are localized to the nucleoplasmic side of the NPC. Rat studies show that the 98 kDa nucleoporin functions as one of several docking site nucleoporins of transport substrates. The human gene has been shown to fuse to several genes following chromosome translocations in acute myelogenous leukemia (AML) and T-cell acute lymphocytic leukemia (T-ALL). This gene is one of several genes located in the imprinted gene domain of 11p15.5, an important tumor-suppressor gene region. Alterations in this region have been associated with the Beckwith-Wiedemann syndrome, Wilms tumor, rhabdomyosarcoma, adrenocortical carcinoma, and lung, ovarian, and breast cancer. Alternative splicing of this gene results in several transcript variants; however, not all variants have been fully described. [provided by RefSeq, May 2010] (from NCBI)
Top mentioned proteins: p15, Nucleoporin, HOXA9, CAN, SP-D
Papers on NUP98
PUMA promotes apoptosis of hematopoietic progenitors driving leukemic progression in a mouse model of myelodysplasia.
Curtis et al., Melbourne, Australia. In Cell Death Differ, Feb 2016
Using the NUP98-HOXD13 (NHD13) transgenic mouse model of MDS, we previously reported that overexpression of the anti-apoptotic protein BCL2, blocked apoptosis and improved cytopenias, paradoxically, delaying leukemic progression.
Nuclear pore protein NUP88 activates anaphase-promoting complex to promote aneuploidy.
van Deursen et al., In J Clin Invest, Feb 2016
We determined that NUP88 and the nuclear transport factors NUP98 and RAE1 comprise a regulatory network that inhibits premitotic activity of the anaphase-promoting complex/cyclosome (APC/C).
Arabidopsis TAF15b localizes to RNA processing bodies and contributes to snc1-mediated autoimmunity.
Germain et al., Vancouver, Canada. In Mol Plant Microbe Interact, Jan 2016
The Arabidopsis nuclear protein MOS11 along with the nucleoporins MOS3/Nup96/SAR3 and Nup160/SAR1 are components of the mRNA export machinery and contribute to immunity mediated by nucleotide binding leucine-rich repeat immune receptors (NLRs).
Formation of Nup98-containing nuclear bodies in HeLa sublines is linked to genomic rearrangements affecting chromosome 11.
Geoffroy et al., Paris, France. In Chromosoma, Jan 2016
UNASSIGNED: Nup98 is an important component of the nuclear pore complex (NPC) and also a rare but recurrent target for chromosomal translocation in leukaemogenesis.
Increased Engraftment of Human Short Term Repopulating Hematopoietic Cells in NOD/SCID/IL2rγnull Mice by Lentiviral Expression of NUP98-HOXA10HD.
Persons et al., Vancouver, Canada. In Plos One, Dec 2015
NUP98-HOXA10HD is a relatively newly discovered fusion gene that in mouse transplant experiments has been shown to increase numbers of hematopoietic stem cells.
Acute Myeloid Leukemia With Myelodysplasia-Related Changes.
Reichard et al., Rochester, United States. In Am J Clin Pathol, Jul 2015
RESULTS: Session 3 of the workshop cases displayed heterogeneity as expected within AML-MRC, yet several cases suggested that recently recognized entities may exist within this category, such as familial MDS/AML predisposition syndromes and rare cases of high-risk AML associated with the cryptic t(5;11)(q35;p15);NUP98-NSD1 that may masquerade as a del(5q).
AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes.
Armstrong et al., Boston, United States. In Cancer Cell, 2015
AF10 inactivation reverses leukemia-associated epigenetic profiles, precludes abnormal HOXA gene expression, and impairs the transforming ability of MLL-AF9, MLL-AF6, and NUP98-NSD1 fusions-mechanistically distinct HOX-activating oncogenes.
Nucleoporins and nucleocytoplasmic transport in hematologic malignancies.
Yaseen et al., Saint Louis, United States. In Semin Cancer Biol, 2014
Rearrangements of the genes encoding two nucleoporins, NUP98 and NUP214, have been implicated in the pathogenesis of several types of hematologic malignancies, particularly acute myeloid leukemia.
Hox gene dysregulation in acute myeloid leukemia.
De Braekeleer et al., Brest, France. In Future Oncol, 2014
Changes in HOX gene expression can be associated with chromosomal rearrangements generating fusion genes, such as those involving MLL and NUP98, or molecular defects, such as mutations in NPM1 and CEBPA for example.
A NUP98-HOXD13 leukemic fusion gene leads to impaired class switch recombination and antibody production.
Caudell et al., Blacksburg, United States. In Exp Hematol, 2012
findings show that expression of NUP98-HOXD13 impairs class switch recombination and reduces the antibody-mediated immune response, in addition to its role in leukemia
Molecular basis for the anchoring of proto-oncoprotein Nup98 to the cytoplasmic face of the nuclear pore complex.
Hoelz et al., Pasadena, United States. In J Mol Biol, 2012
Human Nup98 intereacted with Nup82 through a reciprocal exchange of loop structures. Strikingly, the same Nup98 groove promiscuously interacted with Nup82 and Nup96 in a mutually excusive fashion.
Knock-in of a FLT3/ITD mutation cooperates with a NUP98-HOXD13 fusion to generate acute myeloid leukemia in a mouse model.
Small et al., Baltimore, United States. In Blood, 2012
Mice expressing both the FLT3/ITD and Nup98-HoxD13 (NHD13) fusion gene developed acute myeloid leukemia with 100% penetrance
Functional analysis of the NUP98-CCDC28A fusion protein.
Penard-Lacronique et al., Villejuif, France. In Haematologica, 2012
the recurrent NUP98-CCDC28A is an oncogene that induces a rapid and transplantable myeloid neoplasm in recipient mice. They also provide additional evidence for an alternative leukemogenic mechanism for NUP98 oncogenes.
Expression of the novel NUP98/PSIP1 fusion transcripts in myelodysplastic syndrome with t(9;11)(p22;p15).
Minami et al., Kōbe, Japan. In Eur J Haematol, 2012
The fusion genes combining NUP98 exon 11/12 with PSIP1 exon 8 may be implicated in the pathogenesis of myelodysplastic syndrome (MDS).
NUP98 gene fusions and hematopoietic malignancies: common themes and new biologic insights.
Aplan et al., Bethesda, United States. In Blood, 2012
Structural chromosomal rearrangements of NUP98, primarily balanced translocations and inversions, are associated with wide array of hematopoietic malignancies; NUP98 is known to be fused to at least 28 different partner genes in patients. [REVIEW]
[Recent progress of study on retroviral mediated mouse model of myeloid leukemia --- review].
Chen et al., Shanghai, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2011
Additional genetic events are verified to cooperate with fusion genes resulting from chromosomal translocations in acute myeloid leukemia (AML) to develop a leukemic phenotype in mice, such as C-KIT N822K with AML1-ETO, FLT3-ITD with PML-RARα, Meis1 with NUP98-HOX, and Cdx4 with MLL-AF9.
Regulation of myeloid leukaemia by the cell-fate determinant Musashi.
Reya et al., Durham, United States. In Nature, 2010
As a possible explanation for the decreased levels of Numb in the blast crisis phase, we show that NUP98-HOXA9, an oncogene associated with blast crisis CML, can trigger expression of the RNA-binding protein Musashi2 (Msi2), which in turn represses Numb.
Haematopoietic malignancies caused by dysregulation of a chromatin-binding PHD finger.
Allis et al., New York City, United States. In Nature, 2009
Here we report that fusing an H3K4-trimethylation (H3K4me3)-binding PHD finger, such as the carboxy-terminal PHD finger of PHF23 or JARID1A (also known as KDM5A or RBBP2), to a common fusion partner nucleoporin-98 (NUP98) as identified in human leukaemias, generated potent oncoproteins that arrested haematopoietic differentiation and induced acute myeloid leukaemia in murine models.
Evolution of the Drosophila nuclear pore complex results in multiple hybrid incompatibilities.
Presgraves et al., Rochester, United States. In Science, 2009
Furthermore, the protein encoded by Nup160 directly interacts with that of another hybrid lethality gene, Nup96, indicating that at least two lethal hybrid incompatibility genes have evolved as byproducts of divergent coevolution among interacting components of the Drosophila nuclear pore complex.
Imaging hematopoietic precursor division in real time.
Reya et al., Durham, United States. In Cell Stem Cell, 2007
Oncoproteins can also influence division pattern: although BCR-ABL predominantly alters the rate of division and death, NUP98-HOXA9 promotes symmetric division, suggesting that distinct oncogenes subvert different aspects of cellular function.
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