Aperçu des produits pour Nucleophosmin (Nucleolar phosphoprotein B23, Numatrin) Protéines (NPM1)

Human Nucleophosmin (Nucleolar phosphoprotein B23, Numatrin) (NPM1) interaction partners

1. Study shows that in acute myeloid leukemia (AML) cells loss of NPM1c from the cytoplasm, either through nuclear relocalization or targeted degradation, results in immediate downregulation of homeobox genes followed by differentiation. XPO1 inhibition relocalizes NPM1c to the nucleus, promotes differentiation of AML cells, and prolongs survival of Npm1-mutated leukemic mice.

2. At the time of relapse, NPM1-mut loss acute myeloid leukemia (AML) patients (pts) feature distinct mutational patterns that share almost no somatic mutation with the corresponding diagnosis sample. In contrast, profiles of pts with persistent NPM1-mut are reflected by a high overlap of mutations between diagnosis and relapse suggesting a second "de novo" or treatment-associated AML as alternative cause of relapse.

3. High NMP1 expression is associated with oral cancer.

4. overexpression of INPP4B promotes NPM1-mutated leukemia cell proliferation through SGK3 activation. High levels of INPP4B are at least partially induced by the NPM1 mutant via ERK/Ets-1 signaling.

5. A significant subset of NPM1-mutated myeloid AML has a distinct acute promyelocytic-like immunophenotype, specifically, with negativity for CD34 and HLA-DR and positivity for CD117 and myeloperoxidase, in the absence of PML-RARA, as well as a strong association with TET2 and IDH1/2 mutations. This subset of NPM1-mutated AML was associated with longer relapse-free and overall survival.

6. NCL-NPM complex formation is completely abolished by the mutation and that the presence/absence of the interaction is not affected by drugs causing genotoxic stress or differentiation. Deregulation resulting from changes of NCL/NPMwt ratio may contribute to leukemogenesis.

7. NPM1 gene mutation in AML patients often is accompanied by other gene mutations, while the coexistence of fusion genes is rare

8. Evolution of NPM1-negative therapy-related myelodysplastic syndromes following curative treatment of NPM1-mutant AML.

9. The impact of age, NPM1(mut), and FLT3(ITD) allelic ratio in patients with acute myeloid leukemia.

10. HOTAIR could regulate NPM1 by interacting with miR-646, thereby governing the viability, migration, and invasion of endometrial cancer cells.

11. Nucleophosmin (NPM1) was identified as a binding partner of DDX27 which increased NPM1 protein nuclear translocation. Its knockdown abrogated DDX27-mediated NF-kappaB signaling and colorectal cancer cell growth.

12. The NPM1 gene was the most frequently mutated gene in both white blood cells and cell-free DNA in healthy individuals.

13. NPM1 protein could promote more cells to enter S phase

14. A novel NPM1-interacting motif occurs in the C-terminal region of p14arf, which corresponds to its predicted nucleolar localization signal. This motif recognizes a specific region of the NPM1 N-terminal domain and, upon binding, the 2 proteins form soluble high molecular weight complexes.

15. NPM1 and SURF6 form heterotypic liquid-like droplets in the nucleolus.

16. High NPM1 expression is associated with tongue neoplasms.

17. his meta-analysis indicated that NPM may act as a valuable prognosis biomarker and a potential therapeutic target in human solid tumors.

18. this paper shows that viral nucleocapsid interacts with NPM1 and protects it from proteolytic cleavage, enhancing Cell survival, and is involved in porcine epidemic diarrhea virus growth

19. DNMT3A R882 mutation plays an important role in CN-AML patients' prognosis and clinical outcomes in the presence and absence of NPM1 and FLT3 mutations.

20. Mutation in NPM1 gene is associated with Acute Myeloid Leukemia.

Mouse (Murine) Nucleophosmin (Nucleolar phosphoprotein B23, Numatrin) (NPM1) interaction partners

1. Study shows that in acute myeloid leukemia (AML) cells loss of NPM1c from the cytoplasm, either through nuclear relocalization or targeted degradation, results in immediate downregulation of homeobox genes followed by differentiation. XPO1 inhibition relocalizes NPM1c to the nucleus, promotes differentiation of AML cells, and prolongs survival of Npm1-mutated leukemic mice.

2. In the current study, we demonstrate the existence of a negative feedback loop through which an increased B23 expression suppresses ERalpha. Because suppression of ERalpha expression is a late event during estrogen-dependent endometrial tumorigenesis, the inhibition of nucleophisminmay represent a strategy to promote ERalpha re-expression that ultimately restores tumor sensitivity to hormonal therapy

3. molecular complementarity underlies the higher frequency and significantly worse prognosis associated with NPM1c/FLT3-internal tandem duplications vs NPM1/NRAS-G12D-mutant acute myeloid leukemia (AML) and functionally confirm the role of HOXA genes in NPM1c-driven AML.

4. NPM1-dependent nucleolar PIDDosome is a key initiator of the caspase-2 activation cascade.

5. NPM1 knockdown decreased NF-kappaB-mediated transcription of selected target genes by decreasing the recruitment of NF-kappaB p65 to the gene promoters.

6. study suggests that although neurons need NPM1 for survival, an increase in its expression beyond physiological levels and its translocation to the cytoplasm leads to death through abortive cell cycle induction.

7. The levels of B23 expression are directly regulated by EGR1.

8. IDH2 and NPM1 mutations synergize in the development and maintenance of acute myeloid leukemia stem-like cells.

9. Lrrc34, a novel nucleolar protein, interacts with npm1 and ncl and has an impact on pluripotent stem cells

10. a function of NPM1 in the spatial organization of nucleolus-associated heterochromatin through DNA methyltransferase DNMT3A

11. The data presented here support a novel role for NPM1 as a multilevel modulator of the base excision repair pathway.

12. The mechanism of G-CSF's neuroprotection may be related in part to attenuating neuronal apoptosis by NPM1.

13. In conclusion, we successfully established xenotransplantation model of human FLT3-ITD (mut) /NPM1 (-) CN-AML in NOD/SCID mice.

14. This in vivo model of Flt3/ITD+/NPMc+ leukemia closely recapitulates human disease and will therefore serve as a tool for the investigation of the biology of this common disease entity

15. HOPS acts as a functional bridge in the interaction between NPM and p19(Arf)

16. NPM-Bax interaction enhances mitochondrial Bax accumulation, organelle injury, and cell death.

17. These results suggest that the down-regulation of the identified nucleophosmin proteins in QRsP-11 cells compared to QR-32 cells is possibly related to tumor malignant progression.

18. Overexpression of Npm1 in mice results in myeloproliferation and implies a perturbation in hematopoietic microenvironment.

19. The B23 regulates neuronal survival by preventing SIAH1-GAPDH death signaling under stress-induced conditions in the brain.

20. the aberrant feed-forward pathway that keeps eIF4E and C/EBPalphap30 elevated in NPM1(+/-) cells contributes to the MDS phenotype associated with NPM1 deficiency.

Cow (Bovine) Nucleophosmin (Nucleolar phosphoprotein B23, Numatrin) (NPM1) interaction partners

1. Depletion of B23 expression inhibits virus production by BIV-infected cells, indicating that B23 plays an important role in BIV replication.

2. Results suggest that some polymorphisms in NPM1 are associated with body weight at some ages and may be used as candidates for marker-assisted selection and management in beef cattle breeding programmes.

3. The NPM1 gene is a candidate gene for growth traits in cattle.

Fruit Fly (Drosophila melanogaster) Nucleophosmin (Nucleolar phosphoprotein B23, Numatrin) (NPM1) interaction partners

1. NLP and HMR largely co-localize in domains that are immediately adjacent to, yet distinct from centromere domains defined by the centromeric histone dCENP-A.

2. NLP is essential for the positioning of centromeres during cell division in Drosophila.