Mnt Takes Control as Key Regulator of the Myc/Max/Mxd Network

Wahlström, Therese; Henriksson, Marie Arsenian

doi:10.1016/s0065-230x(06)97003-1

Cited by 25 publications

(23 citation statements)

References 75 publications

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“…Moreover, the TF Rox, also known as the Mnt MAX-binding protein, was also specifically captured by the wild-type probe. This TF, known to act as a key transcriptional regulator of the Myc/Max network, represses transcription by competing with c-Myc for Max-binding and through a well-described direct interaction with Sin3A complex (61,62). These results are consistent with the repressive activity associated with this site.…”

Section: Resultsmentioning

confidence: 99%

Unbiased proteomic analysis of proteins interacting with the HIV-1 5′LTR sequence: role of the transcription factor Meis

Tacheny

Michel

Dieu

et al. 2012

Nucleic Acids Research

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To depict the largest picture of a core promoter interactome, we developed a one-step DNA-affinity capture method coupled with an improved mass spectrometry analysis process focused on the identification of low abundance proteins. As a proof of concept, this method was developed through the analysis of 230 bp contained in the 5′long terminal repeat (LTR) of the human immunodeficiency virus 1 (HIV-1). Beside many expected interactions, many new transcriptional regulators were identified, either transcription factors (TFs) or co-regulators, which interact directly or indirectly with the HIV-1 5′LTR. Among them, the homeodomain-containing TF myeloid ectopic viral integration site was confirmed to functionally interact with a specific binding site in the HIV-1 5′LTR and to act as a transcriptional repressor, probably through recruitment of the repressive Sin3A complex. This powerful and validated DNA-affinity approach could also be used as an efficient screening tool to identify a large set of proteins that physically interact, directly or indirectly, with a DNA sequence of interest. Combined with an in silico analysis of the DNA sequence of interest, this approach provides a powerful approach to select the interacting candidates to validate functionally by classical approaches.

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Section: Resultsmentioning

confidence: 99%

Unbiased proteomic analysis of proteins interacting with the HIV-1 5′LTR sequence: role of the transcription factor Meis

Tacheny

Michel

Dieu

et al. 2012

Nucleic Acids Research

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“…Activation of CaSR also suppresses c‐Myc expression [7]. The E‐box is a major response element in the promoter of the TS gene and c‐Myc binds the E‐box [38, 39]. Thus, the suppression of c‐Myc by CaSR may also directly affect the transcription of the TS gene in a negative manner.…”

Section: Discussionmentioning

confidence: 99%

Nifedipine synergizes with calcium in activating the calcium sensing receptor, suppressing the expression of thymidylate synthase and survivin and promoting sensitivity to fluorouracil in human colon carcinoma cells

Premkumar

Chakrabarty

2011

Molecular Carcinogenesis

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We have previously reported that activation of the G protein coupled calcium-sensing receptor (CaSR) by extracellular Ca(2+) down-modulates the expression of thymidylate synthase (TS) and survivin and promotes sensitivity to fluorouracil in human colon carcinoma cells. Here, we report for the first time that the cardiac drug nifedipine acted synergistically with Ca(2+) in CaSR activation and in the induction of intracellular Ca(2+). Nifedipine in combination with Ca(2+) significantly down-modulated the expression of TS and survivin and promoted sensitivity to 5-FU above and beyond the level achievable with Ca(2+) alone. Nifedipine by itself, however, had no effect on the suppression of TS or survivin or sensitivity to 5-FU. The action of Ca(2+) or in combination with nifedipine was entirely CaSR dependent as the aforementioned effects did not occur in CaSR knocked down cells. siRNAs targeting TS or survivin or both could mimic the effect of CaSR activation in promoting sensitivity to 5-FU. We conclude that nifedipine acts in synergy with Ca(2+) in activating CaSR and in promoting sensitivity to 5-FU by down modulating the expression of TS and survivin. G-protein coupled CaSR has the potential of serving as a target for improving therapeutic outcome in colon cancer.

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“…New AR regulators include the serine/threonine kinase HIPK2 (Rinaldo et al 2007); the lipid kinase DGKI (Raben and Tu-Sekine 2008); nuclear factors PHACTR3 (also known as scapinin), which is an actin and PP1 phosphatase-binding protein associated with the nuclear scaffold (Sagara et al 2003(Sagara et al , 2009); MED19, a component of the Mediator complex (Baidoobonso et al 2007); and MXD1, which competes with MYC for binding to MAX (Wahlstrom and Henriksson 2007). Other factors identified were NUP153, subunit of the nuclear pore complex (Ball and Ullman 2005); DDX39B (also known as BAT1), an RNA helicase involved in mRNA splicing and transport (Peelman et al 1995); HLF (Hunger et al 1992) and CREB1 (Siu and Jin 2007), both bZIP transcription factors; HHEX, a homeobox transcription factor (Bedford et al 1993); and CSTF2T, a pre-mRNA binding protein (Takagaki and Manley 1997).…”

Section: Genome-wide Rnai Screen For New Ar Regulatorsmentioning

confidence: 99%

A genome-wide RNA interference screen identifies new regulators of androgen receptor function in prostate cancer cells

Imberg-Kazdan

Greenfield

et al. 2013

Genome Res.

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The androgen receptor (AR) is a mediator of both androgen-dependent and castration-resistant prostate cancers. Identification of cellular factors affecting AR transcriptional activity could in principle yield new targets that reduce AR activity and combat prostate cancer, yet a comprehensive analysis of the genes required for AR-dependent transcriptional activity has not been determined. Using an unbiased genetic approach that takes advantage of the evolutionary conservation of AR signaling, we have conducted a genome-wide RNAi screen in Drosophila cells for genes required for AR transcriptional activity and applied the results to human prostate cancer cells. We identified 45 AR-regulators, which include known pathway components and genes with functions not previously linked to AR regulation, such as HIPK2 (a protein kinase) and MED19 (a subunit of the Mediator complex). Depletion of HIPK2 and MED19 in human prostate cancer cells decreased AR target gene expression and, importantly, reduced the proliferation of androgen-dependent and castration-resistant prostate cancer cells. We also systematically analyzed additional Mediator subunits and uncovered a small subset of Mediator subunits that interpret AR signaling and affect AR-dependent transcription and prostate cancer cell proliferation. Importantly, targeting of HIPK2 by an FDA-approved kinase inhibitor phenocopied the effect of depletion by RNAi and reduced the growth of AR-positive, but not AR-negative, treatment-resistant prostate cancer cells. Thus, our screen has yielded new AR regulators including drugable targets that reduce the proliferation of castration-resistant prostate cancer cells.

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Mnt Takes Control as Key Regulator of the Myc/Max/Mxd Network

Cited by 25 publications

References 75 publications

Unbiased proteomic analysis of proteins interacting with the HIV-1 5′LTR sequence: role of the transcription factor Meis

Unbiased proteomic analysis of proteins interacting with the HIV-1 5′LTR sequence: role of the transcription factor Meis

Nifedipine synergizes with calcium in activating the calcium sensing receptor, suppressing the expression of thymidylate synthase and survivin and promoting sensitivity to fluorouracil in human colon carcinoma cells

A genome-wide RNA interference screen identifies new regulators of androgen receptor function in prostate cancer cells

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