Plasma cell migration is crucial to immunity, but little is known about the molecular regulators of their migratory programs. Here, we detail the critical role of the transcription factor c-Myb in determining plasma cell location. In the absence of c-Myb, no IgG(+) antigen-specific plasma cells were detected in the bone marrow after immunization or virus infection. This was correlated with a dr...

MiR-150 is a microRNA (miRNA) specifically expressed in mature lymphocytes, but not their progenitors. A top predicted target of miR-150 is c-Myb, a transcription factor controlling multiple steps of lymphocyte development. Combining loss- and gain-of-function gene targeting approaches for miR-150 with conditional and partial ablation of c-Myb, we show that miR-150 indeed controls c-Myb express...

Hexamethylenebisacetamide (HMBA)-induced differentiation of murine erythroleukemia cells (MELC) is a multistep process involving an early latent period during which a number of metabolic changes have been detected, but the cells are not yet committed irreversibly to differentiate. Commitment is defined as the capacity of MELC to go on to express the program of terminal cell division and gene ex...

The synthetic nucleoside analogue, tiazofurin (2-/8-D-ribofuranosylthiazole-4-carboxamide, NSC 286193) is an inhibitor of the enzyme inosine monophosphate (IMP) dehydrogenase and depletes guanine nucleotide pools. In the present study, we have monitored the effects of tiazofurin on human HL-60 promyelocytic cell differentiation and pro tooncogene expression. Tiazofurin (10 ¿IM) induced a more ...

The synthetic nucleoside analogue, tiazofurin (2-beta-D-ribofuranosylthiazole-4-carboxamide, NSC 286193) is an inhibitor of the enzyme inosine monophosphate (IMP) dehydrogenase and depletes guanine nucleotide pools. In the present study, we have monitored the effects of tiazofurin on human HL-60 promyelocytic cell differentiation and protooncogene expression. Tiazofurin (10 microM) induced a mo...

The c-Myb transcription factor regulates the differentiation of immature erythroid, lymphoid, and myeloid cells, although only the latter cells become transformed by the v-myb oncogene. These are also the only cells that express the Myb-regulated gene mim-1, suggesting that Myb requires tissue-specific, cooperating factors to activate such genes. Here, we investigated the tissue-specific regula...

Nemo-like kinase (NLK), a mediator of the Wnt signaling pathway, binds directly to c-Myb, leading to its phosphorylation, ubiquitination and proteasome-dependent degradation. NLK was significantly downregulated in the breast cancer tissues compared to corresponding normal tissues. NLK expression was negatively correlated with c-Myb expression. NLK suppressed proliferation, induced apoptosis and...

Intrinsically disordered proteins often become structured upon interacting with their partners. The mechanism of this 'folding upon binding' process, however, has not been fully characterised yet. Here we present a study of the folding of the intrinsically disordered transactivation domain of c-Myb (c-Myb) upon binding its partner KIX. By determining the structure of the folding transition stat...

BACKGROUND Advanced-stage neuroblastoma resists conventional treatment; hence, novel therapeutic approaches are required. We evaluated the use of c-myb antisense oligodeoxynucleotides (asODNs) delivered to cells via targeted immunoliposomes to inhibit c-Myb protein expression and neuroblastoma cell proliferation in vitro. METHODS Phosphorothioate asODNs and control sequences were encapsulated...

Vertebrates express three different Myb family transcription factors, A-Myb, B-Myb, and c-Myb, that share a highly conserved DNA binding domain, bind to the same DNA sequences, and activate the same reporter gene constructs in transfection assays. However, the three Myb proteins have completely different biological roles, and microarray assays have shown that ectopic expression of each protein ...