JmjC-domain-containing histone demethylases of the JMJD1B type as putative precursors of endogenous DSIP

Mikhaleva, I. I.; Прудченко, И. А.; Иванов, В. Т.; Войтенков, В. Б.

doi:10.1016/j.peptides.2011.01.006

Cited by 11 publications

(5 citation statements)

References 30 publications

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“…JMJD1B, which is a typical JmjC domain-containing protein, was previously characterized as one of the lysine demethylases targeting H3K9 dimethylation ( Kim et al, 2012 ; Mikhaleva et al, 2011 ). We recently found that flap endonuclease 1 (FEN1), which undergoes SDMA at the R192 residue in S phase or in response to DNA damage ( Guo et al, 2010 ), is in complex with JMJD1B.…”

Section: Resultsmentioning

confidence: 99%

JMJD1B Demethylates H4R3me2s and H3K9me2 to Facilitate Gene Expression for Development of Hematopoietic Stem and Progenitor Cells

Ali

Duan³

et al. 2018

Cell Reports

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SUMMARYThe arginine methylation status of histones dynamically changes during many cellular processes, including hematopoietic stem/progenitor cell (HSPC) development. The arginine methyltransferases and the readers that transduce the histone codes have been defined. However, whether arginine demethylation actively occurs in cells and what enzyme demethylates the methylarginine residues during various cellular processes are unknown. We report that JMJD1B, previously identified as a lysine demethylase for H3K9me2, mediates arginine demethylation of H4R3me2s and its intermediate, H4R3me1. We show that demethylation of H4R3me2s and H3K9me2s in promoter regions is correlated with active gene expression. Furthermore, knockout of JMJD1B blocks demethylation of H4R3me2s and/or H3K9me2 at distinct clusters of genes and impairs the activation of genes important for HSPC differentiation and development. Consequently, JMJD1B−/− mice show defects in hematopoiesis. Altogether, our study demonstrates that demethylase-mediated active arginine demethylation process exists in eukaryotes and that JMJD1B demethylates both H4R3me2s and H3K9me2 for epigenetic programming during hematopoiesis.

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Section: Resultsmentioning

confidence: 99%

JMJD1B Demethylates H4R3me2s and H3K9me2 to Facilitate Gene Expression for Development of Hematopoietic Stem and Progenitor Cells

Ali

Duan³

et al. 2018

Cell Reports

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“…However, the DSIP-homologous sequence of the KND peptide originated from the 324-332 fragment, while the only catalytic fragment of JmjC is represented by the 1498-1721 sequence [1], which explains why the search for similarities in the mechanism of action of the human lysine-specific histone demethylase 3B and the KND peptide does not seem appropriate. The functional identity of the KND peptide and DSIP has already been demonstrated [3], and suggests that the mechanisms associated with the activities of DSIP are identical to those for KND.…”

Section: Discussionmentioning

confidence: 75%

“…The same study showed an increase in the rate of oxidative phosphorylation in the mitochondria of the rat brain homogenate, and its results suggest that the protec-tive effects of DSIP in ischemic tissues are due to its influence on the mitochondrial ATP transport system. In our previous studies, the protective effects against cisplatin toxicity were shown for DSIP and were greater for KND [1,3]. The mechanism of the toxic action of cisplatin, which also exhibits anticancer action, was realized through oxidative stress, leading to an increase in the level of free radical oxidation and the resultant DNA damage and dysfunction of the mitochondria that in turn causes apoptosis [46].…”

Section: Discussionmentioning

confidence: 96%

“…Previous studies have demonstrated that the biological activity of the KND peptide is superior to that of DSIP. Thus, the antioxidant and anticonvulsant activity of the KND peptide, as well as its effect on animal behavior, have been shown to be more pronounced in comparison to DSIP [3]. The KND peptide provided a two-fold reduction in the mortality of animals after the administration of anticancer drug cisplatin at a dose of LD 50 [1].…”

Section: Introductionmentioning

confidence: 99%

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DSIP-Like KND Peptide Reduces Brain Infarction in C57Bl/6 and Reduces Myocardial Infarction in SD Rats When Administered during Reperfusion

et al. 2021

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A structural analogue of the DSIP, peptide KND, previously showed higher detoxification efficacy upon administration of the cytotoxic drug cisplatin, compared to DSIP. DSIP and KND were investigated using the model of acute myocardial infarction in male SD rats and the model of acute focal stroke in C57Bl/6 mice. A significant decrease in the myocardial infarction area was registered in KND-treated animals relative to saline-treated control animals (19.1 ± 7.3% versus 42.1 ± 9.2%). The brain infarction volume was significantly lower in animals intranasally treated with KND compared to the control saline-treated animals (7.4 ± 3.5% versus 12.2 ± 5.6%). Injection of KND in the first minute of reperfusion in the models of myocardial infarction and cerebral stroke reduced infarction of these organs, indicating a pronounced cardioprotective and neuroprotective effect of KND and potentiality for the treatment of ischemia-reperfusion injuries after transient ischemic attacks on the heart and brain, when administered during the reperfusion period. A preliminary pilot study using the model of myocardial infarction with the administration of DSIP during occlusion, and the model of cerebral stroke with the administration of KND during occlusion, resulted in 100% mortality in animals. Thus, in the case of ischemia-reperfusion injuries of the myocardium and the brain, use of these peptides is only possible during reperfusion.

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“…It is difficult to understand the role of PinX1 in the clam response against P. olseni; perhaps it is involved in the regulation of the cell proliferation linked to inflammation. Lysine-specific demethylase 3B is a protein involved in fundamental processes of changes in chromatin structure in response to external and internal stress actions, and also regulates processes of cellular growth, differentiation and gene expression in a histone-code-dependent manner (Mikhaleva et al 2011). Its detection in the plasma of clams challenged with P. olseni zoospores deserves further research to assess a specific role in the clam response against this parasite.…”

Section: Discussionmentioning

confidence: 99%

Protein expression profiling in haemocytes and plasma of the Manila clam Ruditapes philippinarum in response to infection with Perkinsus olseni

Fernández-Boo

Villalba

Cao

2016

Journal of Fish Diseases

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The protein expression profiling in clam haemocytes and plasma in response to Perkinsus olseni was addressed. Adult Manila clams from a P. olseni-free bed were experimentally challenged with parasite zoospores to analyse immune response. In another experiment, the effects of longer term infection were assessed in adult clams collected from a P. olseni-affected bed, by comparing moderate to very heavily infected clams with non-infected ones. Haemocyte and plasma proteins were separated by two-dimensional electrophoresis; spot patterns were qualitatively compared between treatments within each experiment and the spots indicating differential protein expression associated with P. olseni challenge or with field infection were processed for protein identification. Fifteen clam proteins (four in haemocytes and eleven in plasma) of which expression was markedly affected by P. olseni were identified. Some of the identified proteins have a well-known role in clam immune response against the parasite, such as lysozyme and lectins. Rho GTPase-activating protein 6 could be a marker of resistance against P. olseni, which should be further studied.

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JmjC-domain-containing histone demethylases of the JMJD1B type as putative precursors of endogenous DSIP

Cited by 11 publications

References 30 publications

JMJD1B Demethylates H4R3me2s and H3K9me2 to Facilitate Gene Expression for Development of Hematopoietic Stem and Progenitor Cells

JMJD1B Demethylates H4R3me2s and H3K9me2 to Facilitate Gene Expression for Development of Hematopoietic Stem and Progenitor Cells

DSIP-Like KND Peptide Reduces Brain Infarction in C57Bl/6 and Reduces Myocardial Infarction in SD Rats When Administered during Reperfusion

Protein expression profiling in haemocytes and plasma of the Manila clam Ruditapes philippinarum in response to infection with Perkinsus olseni

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