Autodisplay: efficient bacterial surface display of recombinant proteins

Jose, Joachim

doi:10.1007/s00253-005-0227-z

Cited by 117 publications

(89 citation statements)

References 48 publications

(81 reference statements)

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“…46 Bacterial autodisplay provides a powerful experimental platform for the analysis of protein-protein interactions and the development of inhibitors. 47,48 Figure 3B shows that bacteria, which express the KIX domain on their surface, were able to bind GFP-Myb but not GFP. The interaction of Myb and the KIX domain is mediated by an LXXLL motif located in the transactivation domain of Myb.…”

Section: Celastrol Disrupts the Myb-p300 Interactionmentioning

confidence: 99%

Targeting acute myeloid leukemia with a small molecule inhibitor of the Myb/p300 interaction

Uttarkar

Dassé

Coulibaly³

et al. 2016

Blood

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129

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Key Points• Inhibition of Myb activity by a small molecule blocks proliferation of AML cells and prolongs survival of mice in an in vivo AML model.The transcription factor Myb plays a key role in the hematopoietic system and has been implicated in the development of leukemia and other human cancers. Inhibition of Myb is therefore emerging as a potential therapeutic strategy for these diseases. However, because of a lack of suitable inhibitors, the feasibility of therapeutic approaches based on Myb inhibition has not been explored. We have identified the triterpenoid Celastrol as a potent low-molecular-weight inhibitor of the interaction of Myb with its cooperation partner p300. We demonstrate that Celastrol suppresses the proliferative potential of acute myeloid leukemia (AML) cells while not affecting normal hematopoietic progenitor cells. Furthermore, Celastrol prolongs the survival of mice in a model of an aggressive AML. Overall, our work demonstrates the therapeutic potential of a small molecule inhibitor of the Myb/p300 interaction for the treatment of AML and provides a starting point for the further development of Myb-inhibitory compounds for the treatment of leukemia and, possibly, other tumors driven by deregulated Myb. (Blood. 2016;127(9):1173-1182 Introduction Myb, the protein encoded by the MYB proto-oncogene, is now recognized as an attractive therapeutic target for the treatment of leukemia and potentially for other human tumors.1 Myb was originally discovered as the cellular progenitor of the transforming v-Myb transduced by avian myeloblastosis virus. 2,3 Myb is expressed in the hematopoietic progenitor cells, where it acts as a transcription factor to control genes important for lineage determination, cell proliferation, and differentiation. 4,5 The analysis of Myb null and conditional knockout mice and of mice bearing hypomorphic Myb alleles has demonstrated that Myb is essential for most hematopoietic lineages. [6][7][8][9][10][11] Myb is also expressed in several nonhematopoietic tissues, 12 such as the colonic crypts, where it controls the proliferation and differentiation of the intestinal stem cells. 13 Recent work has shown that deregulated Myb plays critical roles in leukemias and other types of cancer. Recurrent translocations and duplications of the Myb locus occur in acute lymphoblastic leukemia of young children. [14][15][16] In addition, genomic rearrangements of Myb have been reported in acute myelomonocytic and basophilic leukemia. [17][18][19] Although such rearrangements are relatively rare, they indicate that aberrant Myb expression contributes to the development of leukemia. Importantly, it has now been realized that Myb also plays essential roles in leukemias caused by genetic lesions of other genes, such as leukemias driven by human acute myeloid leukemia (AML) oncogenes. [20][21][22][23][24][25][26] High expression of Myb is a common characteristic of these leukemias and is essential for maintenance of the leukemic cells. This was initially observed in studies with Myb ant...

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Section: Celastrol Disrupts the Myb-p300 Interactionmentioning

confidence: 99%

Targeting acute myeloid leukemia with a small molecule inhibitor of the Myb/p300 interaction

Uttarkar

Dassé

Coulibaly³

et al. 2016

Blood

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129

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“…Bacterial Autodisplay is an efficient system for the expression of recombinant proteins on the outer membrane of Gram-negative bacteria (38,39). Autodisplay provides a powerful experimental platform for various biotechnologic applications, including the analysis of protein-protein interactions and the development of inhibitors (40,41).…”

Section: Development Of An Autodisplay Binding Assay For the Myb-p300mentioning

confidence: 99%

Naphthol AS-E Phosphate Inhibits the Activity of the Transcription Factor Myb by Blocking the Interaction with the KIX Domain of the Coactivator p300

Uttarkar

Dukare

Bopp

et al. 2015

Molecular Cancer Therapeutics

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The transcription factor c-Myb is highly expressed in hematopoietic progenitor cells and controls the transcription of genes important for lineage determination, cell proliferation, and differentiation. Deregulation of c-Myb has been implicated in the development of leukemia and certain other types of human cancer. c-Myb activity is highly dependent on the interaction of the c-Myb with the KIX domain of the coactivator p300, making the disruption of this interaction a reasonable strategy for the development of Myb inhibitors. Here, we have used bacterial Autodisplay to develop an in vitro binding assay that mimics the interaction of Myb and the KIX domain of p300. We have used this binding assay to investigate the potential of Naphthol AS-E phosphate, a compound known to bind to the KIX domain, to disrupt the interaction between Myb and p300. Our data show that Naphthol AS-E phosphate interferes with the Myb-KIX interaction in vitro and inhibits Myb activity in vivo. By using several human leukemia cell lines, we demonstrate that Naphthol AS-E phosphate suppresses the expression of Myb target genes and induces myeloid differentiation and apoptosis. Our work identifies Naphthol AS-E phosphate as the first low molecular weight compound that inhibits Myb activity by disrupting its interaction with p300, and suggests that inhibition of the Myb-KIX interaction might be a useful strategy for the treatment of leukemia and other tumors caused by deregulated c-Myb.

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“…The autotransporter proteins-the peptide chains that 'link' or hold the passenger protein onto the outer membrane of the organism-are common secretion proteins of most Gram-negative bacteria, and are synthesized as precursor protein containing all domains needed to transport the passenger (e.g., cellulases, proteases, lipases, esterases etc.) to the cell surface (Jose 2006;Jose et al 2012). This provides the possibility to transport protein (recombinant or natural passenger) to the outer membrane so long as its coding region lies between a typical signal peptide and a C-terminal "β-barrel" domain (Schumacher et al 2012).…”

Section: Multifunctionalmentioning

confidence: 99%

Lignocellulases: a review of emerging and developing enzymes, systems, and practices

Obeng

Adam

Budiman

et al. 2017

Bioresour. Bioprocess.

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127

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The highly acclaimed prospect of renewable lignocellulosic biocommodities as obvious replacement of their fossilbased counterparts is burgeoning within the last few years. However, the use of the abundant lignocellulosic biomass provided by nature to produce value-added products, especially bioethanol, still faces significant challenges. One of the crucial challenging factors is in association with the expression levels, stability, and cost-effectiveness of the cellulose-degrading enzymes (cellulases). Interestingly, several recommendable endeavors in the bid to curb these challenges are in pursuance. However, the existing body of literature has not well provided the updated roadmap of the advancement and key players spearheading the current success. Moreover, the description of enzyme systems and emerging paradigms with high prospects, for example, the cell-surface display system has been ill-captured in the literature. This review focuses on the lignocellulosic biocommodity pathway, with emphasis on cellulase and hemicellulase systems. The paradigm shift towards cell-surface display system and its emerging recommendable developments have also been discussed. The attempts in supplementing cellulase with other enzymes, accessory proteins, and chemical additives have also been discussed. Moreover, some of the prominent and influential discoveries in the cellulase fraternity have been discussed.

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Autodisplay: efficient bacterial surface display of recombinant proteins

Cited by 117 publications

References 48 publications

Targeting acute myeloid leukemia with a small molecule inhibitor of the Myb/p300 interaction

Targeting acute myeloid leukemia with a small molecule inhibitor of the Myb/p300 interaction

Naphthol AS-E Phosphate Inhibits the Activity of the Transcription Factor Myb by Blocking the Interaction with the KIX Domain of the Coactivator p300

Lignocellulases: a review of emerging and developing enzymes, systems, and practices

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