• Korean Journal of Breeding Science
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• v.42 no.4
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• pp.339-343
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• 2010

Post-translational covalent modifications by small molecules or peptides remodel target proteins. One such modification, made by ubiquitin or small ubiquitin-related modifier (SUMO), is a rapidly expanding field in cell signaling pathways. Ubiquitin attachment controls the turnover and degradation of target proteins while SUMO conjugation regulates their activity and function. Recent studies report many examples of cross-talk between ubiquitin and SUMO pathways, indicating that the boundary is no longer clear. Here, we review recent progress concerning how ubiquitin and SUMO participate in new regulatory roles in plant cell, and how ubiquitination and sumoylation control plant growth and development.

• Proceedings of the Korea Information Processing Society Conference
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• 2010.11a
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• pp.1834-1836
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• 2010

프로테오믹스는 세포 안 또는 개체 안의 모든 단백질을 총체적으로 연구하는 분야이다. 단백질 동정은 단백질이 어떤 아미노산의 서열로 구성되었는지를 확인하는 것이다. 하지만 Post-translational modification과 같은 단백질 변형을 고려하게 되면 단백질 동정은 매우 어렵게 된다. $MOD^i$ 알고리즘은 단백질 동정을 할 때 Post-translational modification의 종류나 개수에 제한 없이 단백질 동정을 정확하게 수행한다. 하지만, 대용량 단백질 서열 데이터베이스를 사용하면 수행시간이 많이 걸리는 단점이 있다. 본 논문에서는 $MOD^i$를 보완하기 위해 대용량 데이터베이스에서 후보 단백질을 선정하는 알고리즘을 통해서 개선된 $MOD^f$ 알고리즘을 제안하고 Target-decoy search strategy를 적용하여 정확성을 분석한다. 후보 단백질 선정 알고리즘과 Target-decoy search strategy 적용 결과 $MOD^f$는 $MOD^i$에 비해 정확도를 희생하지 않으면서 수행속도는 약 2배 향상되었다.

• Journal of Ginseng Research
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• v.25 no.4
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• pp.156-161
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• 2001

We investigated the effects of polyacetylenes of ginseng on farnesyl protein transferase (FPTase) and carboxyl methyl transferase (CMTase) activities related to post-translational modification of Ras protein. We also investigated the effect of petroleum ether extract (PEE) of ginseng on progression of cell cycle. FPTase activity was respectively inhibited 16.2% by 10mM panaxynol and 21.3% by 10mM panaxydol, whereas CMTase activity was not inhibited by panaxynol or panaxydol. Treatment of PEE significantly reduced the numbers and size of human colon cancer cell (HT-29) and human liver cancer cell(HepG2) cultured, respectively. To investigate the mechanism of growth inhibition by PEE of ginseng, we analyzed the cell cycle progressions of PT-29 and HepG2 cells, respectively. We found that PEE significantly inhibited progression of cell cycle from G1 to S phase. These results suggest that anticancer effects of PEE were derived from the arrest of G1 phase in cell cycle progression.

• Journal of Plant Biotechnology
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• v.42 no.4
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• pp.277-283
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• 2015

Plant genome analyses, including Arabidopsis thaliana showed a large gene family of plant receptor kinases with various extracellular ligand-binding domain. Now intensively studies to understand physiological and cellular functions for higher plant receptor kinases in diverse and complex biological processes including plant growth, development, ligands perception including steroid hormone and plant-microbe interactions. Brassinosteroids (BRs) as a one of well know steroid hormone are plant growth hormones that control biomass accumulation and also tolerance to many biotic and abiotic stress conditions and hence are of relevance to agriculture. BRI1 receptor kinase, which is localized in plasma membrane in the cell sense BRs and it bind to a receptor protein known as BRASSINOSTEROID INSENSITIVE 1 (BRI1). Recently, we reported that BRI1 and its co-receptor, BRI1-ASSOCIATED KINASE (BAK1) autophosphorylated on tyrosine residue (s) in vitro and in vivo and thus are dual-specificity kinases. Other plant receptor kinases are also phosphorylated on tyrosine residue (s). Post-translational modifications (PTMs) can be studied by altering the residue modified by directed mutagenesis to mimic the modified state or to prevent the modification. These approaches are useful to not only characterize the regulatory role of a given modification, but may also provide opportunities for plant improvement.

• BMB Reports
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• v.47 no.10
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• pp.593-598
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• 2014

RNA polymerase II carboxyl-terminal domain (RNAPII CTD) phosphatases are responsible for the dephosphorylation of the C-terminal domain of the small subunit of RNAPII in eukaryotes. Recently, we demonstrated the identification of several interacting partners with human small CTD phosphatase1 (hSCP1) and the substrate specificity to delineate an appearance of the dephosphorylation catalyzed by SCP1. In this study, using the established cells for inducibly expressing hSCP1 proteins, we monitored the modification of ${\beta}$-O-linked N-acetylglucosamine (O-GlcNAc). O-GlcNAcylation is one of the most common post-translational modifications (PTMs). To gain insight into the PTM of hSCP1, we used the Western blot, immunoprecipitation, succinylayed wheat germ agglutinin-precipitation, liquid chromatography-mass spectrometry analyses, and site-directed mutagenesis and identified the $Ser^{41}$ residue of hSCP1 as the O-GlcNAc modification site. These results suggest that hSCP1 may be an O-GlcNAcylated protein in vivo, and its N-terminus may function a possible role in the PTM, providing a scaffold for binding the protein(s).

• Molecules and Cells
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• v.41 no.5
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• pp.381-389
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• 2018

ARF is a tumor suppressor protein that has a pivotal role in the prevention of cancer development through regulating cell proliferation, senescence, and apoptosis. As a factor that induces senescence, the role of ARF as a tumor suppressor is closely linked to the p53-MDM2 axis, which is a key process that restrains tumor formation. Thus, many cancer cells either lack a functional ARF or p53, which enables them to evade cell oncogenic stress-mediated cycle arrest, senescence, or apoptosis. In particular, the ARF gene is a frequent target of genetic and epigenetic alterations including promoter hyper-methylation or gene deletion. However, as many cancer cells still express ARF, pathways that negatively modulate transcriptional or post-translational regulation of ARF could be potentially important means for cancer cells to induce cellular proliferation. These recent findings of regulators affecting ARF protein stability along with its low levels in numerous human cancers indicate the significance of an ARF post-translational mechanism in cancers. Novel findings of regulators stimulating or suppressing ARF function would provide new therapeutic targets to manage cancer- and senescence-related diseases. In this review, we present the current knowledge on the regulation and alterations of ARF expression in human cancers, and indicate the importance of regulators of ARF as a prognostic marker and in potential therapeutic strategies.

• BMB Reports
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• v.55 no.7
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• pp.323-335
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• 2022

Together with neuronal loss, the existence of insoluble inclusions of alpha-synuclein (α-syn) in the brain is widely accepted as a hallmark of synucleinopathies including Parkinson's disease (PD), multiple system atrophy, and dementia with Lewy body. Because the α-syn aggregates are deeply involved in the pathogenesis, there have been many attempts to demonstrate the mechanism of the aggregation and its potential causative factors including post-translational modifications (PTMs). Although no concrete conclusions have been made based on the previous study results, growing evidence suggests that modifications such as phosphorylation and ubiquitination can alter α-syn characteristics to have certain effects on the aggregation process in PD; either facilitating or inhibiting fibrillization. In the present work, we reviewed studies showing the significant impacts of PTMs on α-syn aggregation. Furthermore, the PTMs modulating α-syn aggregation-induced cell death have been discussed.

• The Korean Journal of Mycology
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• v.38 no.2
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• pp.89-94
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• 2010

Plant pathogenic fungi are the most diverse and drastic causal agents of crop diseases threatening stable food production all over the world. Plant have evolved efficient innate immune system to scout and counterattack fungal invasion and pathogenic fungi also developed virulence system to nullify plant resistance machinery or signaling pathways and to propagate and dominate within their niche. A growing body of evidences suggests that post translational modifications (PTMs) and selective/nonselective degradations of proteins involved in virulence expression of plant pathogenic fungi and plant defense machinery should play pivotal roles during the compatible and incompatible interactions. This review elucidates recent investigations about the effects of PTMs and protein degradations on host defense and fungal pathogens' invasions.

• IMMUNE NETWORK
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• v.23 no.3
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• pp.25.1-25.17
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• 2023

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces excessive pro-inflammatory cytokine release and cell death, leading to organ damage and mortality. High-mobility group box 1 (HMGB1) is one of the damage-associated molecular patterns that can be secreted by pro-inflammatory stimuli, including viral infections, and its excessive secretion levels are related to a variety of inflammatory diseases. Here, the aim of the study was to show that SARS-CoV-2 infection induced HMGB1 secretion via active and passive release. Active HMGB1 secretion was mediated by post-translational modifications, such as acetylation, phosphorylation, and oxidation in HEK293E/ACE2-C-GFP and Calu-3 cells during SARS-CoV-2 infection. Passive release of HMGB1 has been linked to various types of cell death; however, we demonstrated for the first time that PANoptosis, which integrates other cell death pathways, including pyroptosis, apoptosis, and necroptosis, is related to passive HMGB1 release during SARS-CoV-2 infection. In addition, cytoplasmic translocation and extracellular secretion or release of HMGB1 were confirmed via immunohistochemistry and immunofluorescence in the lung tissues of humans and angiotensin-converting enzyme 2-overexpressing mice infected with SARS-CoV-2.

• Animal cells and systems
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• v.16 no.1
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• pp.1-10
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• 2012

Most living organisms synchronize their physiological and behavioral activities with the daily changes in the environment using intrinsic time-keeping systems called circadian clocks. In mammals, the key molecular features of the internal clock are transcription- and translational-based negative feedback loops, in which clock-specific transcription factors activate the periodic expression of their own repressors, thereby generating the circadian rhythms. CLOCK and BMAL1, the basic helix-loop-helix (bHLH)/PAS transcription factors, constitute the positive limb of the molecular clock oscillator. Recent investigations have shown that various levels of posttranslational regulation work in concert with CLOCK/BMAL1 in mediating circadian and cellular stimuli to control and reset the circadian rhythmicity. Here we review how the CLOCK and BMAL1 activities are regulated by intracellular distribution, posttranslational modification, and the recruitment of various epigenetic regulators in response to circadian and cellular signaling pathways.