Nucleophosmin Recombinant Rabbit Monoclonal Antibody [PD00-91] (HA721206)

UNIPROT #

P06748

PROTEIN NAME

Nucleophosmin

SYNONYMS

B23 antibody;MGC104254 antibody;NO38 antibody;NPM antibody;NPM_HUMAN antibody;NPM1 antibody;Nucleolar phosphoprotein B23 antibody;Nucleolar protein NO38 antibody;Nucleophosmin (nucleolar phosphoprotein B23 numatrin) antibody;Nucleophosmin antibody;nucleophosmin nucleoplasmin family member 1 antibody;Nucleophosmin/nucleoplasmin family member 1 antibody;Numatrin antibody;OTTHUMP00000161024 antibody;OTTHUMP00000161025 antibody;OTTHUMP00000223397 antibody;OTTHUMP00000223398 antibody

SUBCELLULAR LOCATION

Nucleus, nucleolus, nucleoplasm, cytoplasm, cytoskeleton, microtubule organizing center, centrosome.

FUNCTION

Involved in diverse cellular processes such as ribosome biogenesis, centrosome duplication, protein chaperoning, histone assembly, cell proliferation, and regulation of tumor suppressors p53/TP53 and ARF. NPM1 gene is up-regulated, mutated and chromosomally translocated in many tumor types. Chromosomal aberrations involving NPM1 were found in patients with non-Hodgkin lymphoma, acute promyelocytic leukemia, myelodysplastic syndrome, and acute myelogenous leukemia. Heterozygous mice for NPM1 are vulnerable to tumor development. In solid tumors NPM1 is frequently found overexpressed, and it is thought that NPM1 could promote tumor growth by inactivation of the tumor suppressor p53/ARF pathway; on the contrary, when expressed at low levels, NPM1 could suppress tumor growth by the inhibition of centrosome duplication. Of high importance is NPM involvement in acute myelogenous leukemia, where a mutated protein lacking a folded C-terminal domain (NPM1c+) has been found in the cytoplasm in patients. This aberrant localization has been linked to the development of the disease, and is associated with improved clinical outcomes. Strategies against this subtype of acute myelogenous leukemia include the refolding of the C-terminal domain using pharmalogical chaperones and the displacement of the protein from nucleolus to nucleoplasm, which has been linked to apoptotic mechanisms. It has also been shown that in the context of clonal hematopoiesis of undetermined significance harboring a DNMT3A mutation, subsequent NPM1 mutations drive progression into overt myeloproliferative neoplasm.