Trans-2-phenylcyclopropylamine induces nerve cells apoptosis in zebrafish mediated by depression of LSD1 activity

Zhang, Jie; Li, Tan; Jia-Yun, Hou; Qiu, Jiang; Ping-Yao, Zen; Song, Houyan

doi:10.1016/j.brainresbull.2009.04.013

Cited by 23 publications

(17 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We disrupted LSD1 function by using specific siRNAs for LSD1 and BHC80 (Fig. 1c), as well as by using an LSD1 inhibitor, tranylcypromine (TC, also known as trans-2-phenylcyclopropylamine)1718192021, in adipocyte-differentiating 3T3-L1 cells. TC was initially identified as an inhibitor of monoamine oxidases (MAO) A and B22, and was demonstrated to be a potent inhibitor of LSD1 (refs 17,18).…”

Section: Resultsmentioning

confidence: 99%

FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure

et al. 2012

View full text Add to dashboard Cite

Environmental factors such as nutritional state may act on the epigenome that consequently contributes to the metabolic adaptation of cells and the organisms. The lysine-specific demethylase-1 (LSD1) is a unique nuclear protein that utilizes flavin adenosine dinucleotide (FAD) as a cofactor. Here we show that LSD1 epigenetically regulates energy-expenditure genes in adipocytes depending on the cellular FAD availability. We find that the loss of LSD1 function, either by short interfering RNA or by selective inhibitors in adipocytes, induces a number of regulators of energy expenditure and mitochondrial metabolism such as PPARγ coactivator-1α resulting in the activation of mitochondrial respiration. In the adipose tissues from mice on a high-fat diet, expression of LSD1-target genes is reduced, compared with that in tissues from mice on a normal diet, which can be reverted by suppressing LSD1 function. Our data suggest a novel mechanism where LSD1 regulates cellular energy balance through coupling with cellular FAD biosynthesis.

show abstract

Section: Resultsmentioning

confidence: 99%

FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Accordingly, treatment of embryos with the Lsd1 inhibitor trans-2-phenylcyclopropylamine (PCPA) (Jie et al, 2009; Lee et al, 2006) caused a 1.6- to 1.8-fold decrease in the number of OR-positive cells (Figure 6B and Table 2). Together these observations demonstrate that H3K9 demethylation is both necessary and sufficient to activate OR gene expression and further identify the specific involvement of the histone modifying enzymes G9a/GLP and Lsd1 in this process (see also (Lyons et al, 2013)).…”

Section: Resultsmentioning

confidence: 99%

Silencing of Odorant Receptor Genes by G Protein βγ Signaling Ensures the Expression of One Odorant Receptor per Olfactory Sensory Neuron

Ferreira

Wilson

Choi

et al. 2014

Neuron

View full text Add to dashboard Cite

Summary Olfactory sensory neurons express just one out of a possible ~1000 odorant receptor genes, reflecting an exquisite mode of gene regulation. In one model, once an odorant receptor is chosen for expression, other receptor genes are suppressed by a negative feedback mechanism, ensuring a stable functional identity of the sensory neuron for the lifetime of the cell. The signal transduction mechanism subserving odorant receptor gene silencing remains obscure, however. Here we demonstrate in the zebrafish that odorant receptor gene silencing is dependent on receptor activity. Moreover, we show that signaling through G protein βγ subunits is both necessary and sufficient to suppress the expression of odorant receptor genes, and likely acts through histone methylation to maintain the silenced odorant receptor genes in transcriptionally inactive heterochromatin. These results provide new insights linking receptor activity with the epigenetic mechanisms responsible for ensuring the expression of one odorant receptor per olfactory sensory neuron.

show abstract

“…18 Interestingly, according to other recent studies, LSD1 can either render tumor cells resistant to DNA damage or reversely prompt cells to undergo apoptosis in different biological settings, indicating that LSD1 plays a role in cell survival. [23][24][25][26] As mentioned, one of the critical oncogenic roles of Snail lies in apoptosis protection notably through transcriptional repression of PTEN, which serves as a negative regulator of Akt signaling. It would be interesting to find out if LSD1 is involved in Snail-mediated PTEN suppression and cell survival.…”

Section: Introductionmentioning

confidence: 99%

Doxorubicin enhances Snail/LSD1-mediated PTEN suppression in a PARP1-dependent manner

2014

View full text Add to dashboard Cite

Trans-2-phenylcyclopropylamine induces nerve cells apoptosis in zebrafish mediated by depression of LSD1 activity

Cited by 23 publications

References 33 publications

FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure

FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure

Silencing of Odorant Receptor Genes by G Protein βγ Signaling Ensures the Expression of One Odorant Receptor per Olfactory Sensory Neuron

Doxorubicin enhances Snail/LSD1-mediated PTEN suppression in a PARP1-dependent manner

Contact Info

Product

Resources

About