The Runx3 transcription factor regulates development and survival of TrkC dorsal root ganglia neurons

Levanon, Ditsa

doi:10.1093/emboj/cdf370

Cited by 396 publications

(457 citation statements)

References 54 publications

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“…When immunodeficient mice lacking the recombinase Rag2 were reconstituted with fetal liver cells from Runx3 À/À mice, CD4 was derepressed in the peripheral cytotoxic T cells (Taniuchi et al, 2002). Similar results were obtained using a strain of Runx3 knockout mice that are viable for several months (Levanon et al, 2002). These mice displayed reduced numbers of CD8 þ T cells in the thymus and in the circulating T-cell population along with increased expression of CD4 in the peripheral CD8 þ cells (Woolf et al, 2003).…”

Section: Runx-mediated Gene Silencing In Micesupporting

confidence: 56%

Role of RUNX family members in transcriptional repression and gene silencing

2004

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RUNX family members are DNA-binding transcription factors that regulate the expression of genes involved in cellular differentiation and cell cycle progression. The RUNX family includes three mammalian RUNX proteins (RUNX1, -2, -3) and two homologues in Drosophila. Experiments in Drosophila and mouse indicate that the RUNX proteins are required for gene silencing of engrailed and CD4, respectively. RUNX-mediated repression involves recruitment of corepressors such as mSin3A and Groucho as well as histone deacetylases. Furthermore, RUNX1 and RUNX3 associate with SUV39H1, a histone methyltransferase involved in gene silencing. RUNX1 is frequently targeted in human leukemia by chromosomal translocations that fuse the DNA-binding domain of RUNX1 to other transcription factors and corepressor molecules. The resulting leukemogenic fusion proteins are transcriptional repressors that form stable complexes with corepressors, histone deacetylases and histone methyltransferases. Thus, transcriptional repression and gene silencing through RUNX1 contribute to the mechanisms of leukemogenesis of the fusion proteins. Therapies directed at the associated cofactors may be beneficial for treatment of these leukemias.

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Section: Runx-mediated Gene Silencing In Micesupporting

confidence: 56%

Role of RUNX family members in transcriptional repression and gene silencing

2004

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“…Though LMO1 was originally isolated as a candidate oncogene for T-cell acute lymphoblastic leukemia (McGuire et al, 1989;Rabbitts, 1998), our study disclosed a crucial role of LMO1 in gastric epithelium differentiation and it may be also involved in gastric carcinogenesis. Recently, phenotypic discrepancies between two Runx3-KO mice gave rise to some argument about the function of Runx3 in the gastric epithelium (Levanon et al, 2002(Levanon et al, , 2003Li et al, 2002;Bae and Ito, 2003). Moreover, it was reported that Runx3 is not expressed in the gastric epithelium (Levanon et al, 2001), which negates the involvement of Runx3 in gastric carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

GASDERMIN, suppressed frequently in gastric cancer, is a target of LMO1 in TGF-β-dependent apoptotic signalling

Saeki¹,

et al. 2007

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Defining apoptosis-regulatory cascades of the epithelium is important for understanding carcinogenesis, since cancer cells are considered to arise as a result of the collapse of the cascades. We previously reported that a novel gene GASDERMIN (GSDM) is expressed in the stomach but suppressed in gastric cancer cell lines. Furthermore, in this study, we demonstrated that GSDM is expressed in the mucus-secreting pit cells of the gastric epithelium and frequently silenced in primary gastric cancers. We found that GSDM has a highly apoptotic activity and its expression is regulated by a transcription factor LIM domain only 1 (LMO1) through a sequence to which Runt-related transcription factor 3 (RUNX3) binds, in a GSDM promoter region. We observed coexpression of GSDM with LMO1, RUNX3 and type II transforming growth factor-b receptor (TGF-bRII) in the pit cells, and found that TGF-b upregulates the LMO1-and GSDMexpression in the gastric epithelial cell line and induces apoptosis, which was confirmed by the finding that the apoptosis induction is inhibited by suppression of each LMO1-, RUNX3-and GSDM expression, respectively. The present data suggest that TGF-b, LMO1, possibly RUNX3, and GSDM form a regulatory pathway for directing the pit cells to apoptosis.

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“…Transfection efficiencies were normalized by cotransfection with the pCMV-␤gal plasmid, and ␤-galactosidase levels were determined using the Galacto-Light kit (Tropix). The CD36-based reporter gene constructs pCD36-158-luc (CD36Luc) and pCD36-158(m-102/-98)-luc (represented as CD36Luc-98mut) have been previously described (20). CD36Luc contains the Ϫ158/ϩ43 fragment of the CD36 proximal promoter driving the expression of the firefly luciferase cDNA, while CD36Luc-98mut contains a mutated RUNX-binding site (at Ϫ98).…”

Section: Transfections Plasmids and Site-directed Mutagenesismentioning

confidence: 99%

RUNX3 Negatively Regulates CD36 Expression in Myeloid Cell Lines

Puig‐Kröger

Domínguez-Soto

Martínez-Muñoz

et al. 2006

The Journal of Immunology

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CD36 is a member of the scavenger receptor type B family implicated in the binding of lipoproteins, phosphatidylserine, thrombospondin-1, and the uptake of long-chain fatty acids. On mononuclear phagocytes, recognition of apoptotic cells by CD36 contributes to peripheral tolerance and prevention of autoimmunity by impairing dendritic cell (DC) maturation. Besides, CD36 acts as a coreceptor with TLR2/6 for sensing microbial diacylglycerides, and its deficiency leads to increased susceptibility to Staphylococcus aureus infections. The RUNX3 transcription factor participates in reprogramming DC transcription after pathogen recognition, and its defective expression leads to abnormally accelerated DC maturation. We present evidence that CD36 expression is negatively regulated by the RUNX3 transcription factor during myeloid cell differentiation and activation. In molecular terms, RUNX3 impairs the activity of the proximal regulatory region of the CD36 gene in myeloid cells through in vitro recognition of two functional RUNX-binding elements. Moreover, RUNX3 occupies the CD36 gene proximal regulatory region in vivo, and its overexpression in myeloid cells results in drastically diminished CD36 expression. The down-regulation of CD36 expression by RUNX3 implies that this transcription factor could impair harmful autoimmune responses by contributing to the loss of pathogen- and apoptotic cell-recognition capabilities by mature DCs.

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The Runx3 transcription factor regulates development and survival of TrkC dorsal root ganglia neurons

Cited by 396 publications

References 54 publications

Role of RUNX family members in transcriptional repression and gene silencing

Role of RUNX family members in transcriptional repression and gene silencing

GASDERMIN, suppressed frequently in gastric cancer, is a target of LMO1 in TGF-β-dependent apoptotic signalling

RUNX3 Negatively Regulates CD36 Expression in Myeloid Cell Lines

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