A Novel Role of the Mad Family Member Mad3 in Cerebellar Granule Neuron Precursor Proliferation

Yun, Jun Soo; Rust, Jennifer; Ishimaru, Tatsuto; Díaz, Elizabeth

doi:10.1128/mcb.00656-06

Cited by 36 publications

(78 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MXD3 and MNT are interesting exceptions to this inverse pattern of MYC and MXD expression in that they are both expressed during cell proliferation. MNT is present, coincident with MYC, throughout the cell cycle and persists following differentiation, whereas MXD3 expression is restricted to cells in S phase (Queva et al 2001;Yun et al 2007). …”

Section: Regulation Of Myc and Mxd Expressionmentioning

confidence: 99%

An Overview of MYC and Its Interactome

Conacci‐Sorrell

McFerrin

Eisenman

2014

Cold Spring Harbor Perspectives in Medicine

358

398

View full text Add to dashboard Cite

This review is intended to provide a broad outline of the biological and molecular functions of MYC as well as of the larger protein network within which MYC operates. We present a view of MYC as a sensor that integrates multiple cellular signals to mediate a broad transcriptional response controlling many aspects of cell behavior. We also describe the larger transcriptional network linked to MYC with emphasis on the MXD family of MYC antagonists. Last, we discuss evidence that the network has evolved for millions of years, dating back to the emergence of animals.

show abstract

Section: Regulation Of Myc and Mxd Expressionmentioning

confidence: 99%

An Overview of MYC and Its Interactome

Conacci‐Sorrell

McFerrin

Eisenman

2014

Cold Spring Harbor Perspectives in Medicine

358

398

View full text Add to dashboard Cite

show abstract

“…It is an atypical member of the MAD family [13][14][15] , and it has been reported to be involved in carcinogenesis 16,17 . When compared to pBABEpuro (negative control) and MYC (positive control), the NIH 3T3 dishes where MXD3 was overexpressed had significantly less foci ( Figure 1A).…”

Section: Representative Resultsmentioning

confidence: 99%

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Alvarez

Barisone

Díaz

2014

JoVE

View full text Add to dashboard Cite

show abstract

“…It is an ideal target for Abbased therapy against B-cell malignancies because of its high expression and rapid internalization upon Ab binding (17,42,43). MAX dimerization protein 3 (MXD3) is a basic-helix-loop-helix-leucine-zipper transcription factor that is part of the v-myc avian myelocytomatosis viral oncogene homolog (MYC)/MAX/MXD transcriptional network involved in cellular proliferation (44)(45)(46). Previously, we demonstrated that MXD3 functions as an anti-apoptotic protein and that knockdown of MXD3 can be a novel effective therapeutic strategy for preB ALL in vitro (47,48).…”

Section: Cd22 Ab-aso Conjugatementioning

confidence: 99%

Novel Targeted Therapy for Precursor B-Cell Acute Lymphoblastic Leukemia: Anti-CD22 Antibody-MXD3 Antisense Oligonucleotide Conjugate

Satake

Duong

Yoshida

et al. 2016

Mol Med

View full text Add to dashboard Cite

The exponential rise in molecular and genomic data has generated a vast array of therapeutic targets. Oligonucleotide-based technologies to down regulate these molecular targets have promising therapeutic efficacy. However, there is relatively limited success in translating this into effective in vivo cancer therapeutics. The primary challenge is the lack of effective cancer cell-targeted delivery methods, particularly for a systemic disease such as leukemia. We developed a novel leukemiatargeting compound composed of a monoclonal antibody directly conjugated to an antisense oligonucleotide (ASO). Our compound uses an ASO that specifically targets the transcription factor MYC-associated factor X (MAX) dimerization protein 3 (MXD3), which was previously identified to be critical for precursor B-cell (preB) acute lymphoblastic leukemia (ALL) cell survival. The MXD3 ASO was conjugated to an anti-cluster of differentiation-22 (CD22) antibody (αCD22 Ab) that specifically targets most preB ALL. We demonstrated that the αCD22 Ab-ASO conjugate treatment showed MXD3 protein knockdown and leukemia cell apoptosis in vitro. We also demonstrated that the conjugate treatment showed cytotoxicity in normal B cells, but not in other hematopoietic cells, including hematopoietic stem cells. Furthermore, the conjugate treatment at the lowest dose tested (0.2 mg/kg Ab for 6 doses -twice a week for 3 wks) more than doubled the mouse survival time in both Reh (median survival time 20.5 versus 42.5 d, p < 0.001) and primary preB ALL (median survival time 29.3 versus 63 d, p < 0.001) xenograft models. Our conjugate that uses αCD22 Ab to target the novel molecule MXD3, which is highly expressed in preB ALL cells, appears to be a promising novel therapeutic approach.

show abstract

A Novel Role of the Mad Family Member Mad3 in Cerebellar Granule Neuron Precursor Proliferation

Cited by 36 publications

References 61 publications

An Overview of MYC and Its Interactome

An Overview of MYC and Its Interactome

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Novel Targeted Therapy for Precursor B-Cell Acute Lymphoblastic Leukemia: Anti-CD22 Antibody-MXD3 Antisense Oligonucleotide Conjugate

Contact Info

Product

Resources

About