NUP98 Antibody

1. NHA9 (NUP98-HOXA9 fusion protein) deregulates the expression of key leukemic genes, including MEIS1-HOXA9-PBX3 complex, through the enhancer binding and the direct interaction of the fusion protein with HDAC and p300 transcriptional regulators PMID:28630438
2. human NUP98-IQCG fusion protein could induce fatal and transplantable acute myelomonocytic leukemia in a mouse model PMID:26675333
3. Importantly, binding of Nup98 to DHX9 stimulates the ATPase activity of DHX9, and a transcriptional reporter assay suggests Nup98 supports DHX9-stimulated transcription. PMID:28221134
4. The second FG repeat domain of the NUP98 moiety of the NUP98-HOXA9 fusion protein is important for its cell immortalization and leukemogenesis activities. NUP98-HOXA9 interacts with mixed lineage leukemia (MLL) via this FG repeat domain and that, in MLL-null mice, NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. PMID:28210005
5. DYNLT1 interacts with nucleoporins and plays a role in the dysregulation of gene expression and induction of hematopoietic cell proliferation by the leukemogenic nucleoporin fusion, NUP98-HOXA9 PMID:23840580
6. the mutation order in the NUP98-rearranged pediatric AML begins with the NUP98 rearrangement leading to epigenetic dysregulations then followed by mutations of critical hematopoietic transcription factors and finally, activation of the FLT3 signaling pathway. PMID:27694926
7. These results provide novel insight into the mechanisms underlying the aberrant capability of NUP98 oncoproteins to interact with APC/C(Cdc20) and to interfere with its function. PMID:27097363
8. Our results suggest that NA10HD increases the number of gamma-globin-transduced HSCs that engraft, leading to an elevated number of fetal hemoglobin-containing red cells. PMID:28190779
9. NUP98-HOXA9 ability to induce blood cell expansion is evolutionarily conserved. PMID:27838340
10. The study demonstrated the association of NUP98-IQCG with CRM1, and found that NUP98-IQCG expression inhibits the CRM1-mediated nuclear export of p65 and enhances the transcriptional activity of nuclear factor-kappaB. Moreover, IQCG could be entrapped in the nucleus by NUP98-IQCG, and the fusion protein interacts with calmodulin via the IQ motif in a calcium-independent manner. PMID:27864780
11. The results indicate that highly selective targeting of Nup98-fusion proteins to Hox cluster regions via prebound Crm1 induces the formation of higher order chromatin structures that causes aberrant Hox gene regulation. PMID:26740045
12. Despite the difference in localization, all tested Nup98 chimera provoked morphological alterations in the nuclear envelope (NE), in particular affecting the nuclear lamina and the lamina-associated polypeptide 2alpha. PMID:27031510
13. NUP98-HOXA9 expression induces myeloid disease. PMID:26017032
14. Overall, these results demonstrate a novel role for FOXK1 in regulating the expression of antiviral genes via Nup98, from insects to humans. PMID:25852164
15. deregulation of the retinoid/rexinoid signaling pathway has a major role and may represent a potential therapeutic target for NUP98-RARG-mediated transformation PMID:25510432
16. Acute myeloid leukemia can be reproduced in mice by transducing mouse mesenchymal stem cells with the human NUP98-NSD1 fusion and the FLT3-ITD mutated constracts. PMID:24951466
17. These data reveal an emergent Kap-centric barrier mechanism that may underlie mechanistic and kinetic control in the nuclear pore complex. PMID:24739174
18. Vesiculoviral matrix (M) protein occupies nucleic acid binding site at nucleoporin pair (Rae1 * Nup98). PMID:24927547
19. NUP98 oncoproteins predispose myeloid cells to oncogenic transformation or malignant progression by promoting whole chromosome instability. PMID:24371226
20. NUP98/JARID1A is a novel recurrent genetic abnormality in pediatric AMKL PMID:23531517
21. Data indicate increased levels of reactive oxygen species (ROS) were detected in bone marrow nucleated cells (BMNC) that express CD71 in in NUP98-HOXD13 (NHD13) transgenic mice, a murine model for myelodysplastic syndromes (MDS). PMID:23958061
22. support to the adoption of screening for NUP98-NSD1 in pediatric AML without otherwise favorable genetic markers PMID:23999921
23. The repeat domain of Nup98 is substantially more cohesive than repeat domains from other nucleoporins. PMID:23427268
24. Dominant negative Nup98 fusion proteins disrupt the transcriptional activity of wild-type Nup98 in the nucleoplasm to drive acute myeloid leukemia. PMID:23246429
25. Nup98 RNA interference significantly suppresses downstream mRNA expression in the ss-catenin pathway, while nuclear galectin-3 binds to ss-catenin to inhibit transcriptional activity. PMID:23541576
26. This work demonstrates for the first time that NUP98 dynamically associates with the human genome during differentiation, revealing a role of a nuclear pore protein in regulating developmental gene expression programs. PMID:23468646
27. The roles of NUP153 and nup98 in the integration and replication of HIV-1 in human Jurkat lymphocytes are reported. PMID:23523133
28. vesicular stomatitis virus M protein interacted efficiently with Rae1-Nup98 complexes associated with the chromatin fraction of host nuclei, consistent with an effect on host transcription PMID:23028327
29. NUP98/NSD1 fusions are rare in adult acute myeloid leukemia. PMID:22929522
30. Positive NUP98-NSD1 fusion is associated with acute myeloid leukemia. PMID:22945772
31. Nup98 functions as a potential tumor suppressor and regulates posttranscriptional expression of select p53 target genes. PMID:23102701
32. 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 PMID:22613470
33. 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. PMID:22480613
34. 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. PMID:22058212
35. The fusion genes combining NUP98 exon 11/12 with PSIP1 exon 8 may be implicated in the pathogenesis of myelodysplastic syndrome (MDS). PMID:22103895
36. RAE1 transgene may be directly involved in NUP98 fusion-mediated leukemogenesis. PMID:21467841
37. 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] PMID:21948299
38. NUP98/NSD1 identifies a previously unrecognized group of young AML patients, with distinct characteristics and dismal prognosis, for whom new treatment strategies are urgently needed. PMID:21813447
39. Ectopic expression of NA10 (Nup98-HoxA10) augments erythroid differentiation of human embryonic stem cells. PMID:21328509
40. Study identified mitotic phosphorylation of Nup98 as a rate-limiting step in mitotic nuclear pore complexes disassembly. PMID:21335236
41. NUP98/RARG gene rearrangement is associated with acute myeloid leukemia. PMID:20935257
42. results suggest high frequency of cell proliferation gene mutations may contribute to leukemogenesis in NUP98-related leukemia; simultaneous occurrence of FLT3-ITD and WT1 aberrations may have an important role in outcome of NUP98-related leukemia PMID:20861915
43. characterized a novel recurrent chromosomal aberration, inv(11)(p15q23) in 2 patients with acute myeloid leukemia. This aberration is predicted to result in the expression of a NUP98-MLL fusion protein that is unable to interact with menin. PMID:20558618
44. Mapping tests further demonstrated that aa 22-53 in the N-terminal region of H5N1 virus NS2 and the glycine-leucine-phenylalanine-glycine (GLFG) repeat domain (aa 1-511) of human Nup98 are crucial for the interaction of these two proteins. PMID:20554795
45. Findings suggest new possibilities for misregulation by which Nup98 translocations may contribute to cellular transformation and leukemogenesis. PMID:20237156
46. present the crystal structure of human Rae1 in complex with the Gle2-binding sequence (GLEBS) of Nup98 at 1.65 A resolution. Rae1 forms a seven-bladed beta-propeller with several extensive surface loops. PMID:20498086
47. NUP98-DDX10 dramatically increases proliferation and results in leukemogenesis. PMID:20339440
48. Oxidative stress up-regulated the binding of Crm1 to Ran and affected multiple repeat-containing nucleoporins by changing their localization, phosphorylation, O-glycosylation, or interaction with other transport components. PMID:19828735
49. effects of NUP98-HOXA9 on gene transcription and cell transformation are mediated by two distinct mechanisms: promoter binding through homeodomain with direct transcriptional activation, and another depending on NUP98 moiety not involving DNA binding PMID:19696924
50. These results are consistent with a specific proteolysis of Nup98 by 2A protease to prevent de novo mRNA traffic in poliovirus-infected cells. PMID:19789179

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HGNC: 8068

UNIGENE: Hs.524750

KEGG: hsa:4928

STRING: 9606.ENSP00000316032

OMIM: 601021