• Journal of Life Science
• /
• v.17 no.2 s.82
• /
• pp.235-240
• /
• 2007

AvrRpt2 protein triggers hypersensitive response (HR) and strong disease resistance when it is translocated from a bacterial pathogen Pseudomonas sp. to host plant cells containing a cognate RPS2 resistance protein through Type III Secretion System (TTSS). However, AvrRpt2 protein can function as the effector that suppresses a basal defense and enhances the disease symptom when functional RPS2 resistance protein is absent in the infected plant cells. Using Affymetrix Arabidopsis DNA chip, we found that many genes were specifically regulated by AvrRpt2 protein in the rps2 Arabidopsis mutant. Here, we showed that expression of AtERF11 that is known as a member of B1a subcluster of AP2/ERF transcription factor family was down regulated specifically by AvrRpt2. To determine its function in plant resistance, we also generated the Arabidopsis thaliana transgenic plants constitutively overexpressing AtERF11 under CaMV 355 promoter, which conferred an enhanced resistance against a bacterial pathogen, Pseudomonas syringae pv. tomato DC3000. Thus, these results collectively suggest that AtERF11 plays a role as a positive regulator for disease resistance against biotrophic bacterial pathogen in plant.

• Biomolecules & Therapeutics
• /
• v.26 no.6
• /
• pp.533-538
• /
• 2018

Nitric oxide (NO) mediates various physiological and pathological processes, including cell proliferation, differentiation, and inflammation. Protein S-nitrosylation (SNO), a NO-mediated reversible protein modification, leads to changes in the activity and function of target proteins. Recent findings on protein-protein transnitrosylation reactions (transfer of an NO group from one protein to another) have unveiled the mechanism of NO modulation of specific signaling pathways. The intracellular level of S-nitrosoglutathione (GSNO), a major reactive NO species, is controlled by GSNO reductase (GSNOR), a major regulator of NO/SNO signaling. Increasing number of GSNOR-related studies have shown the important role that denitrosylation plays in cellular NO/SNO homeostasis and human pathophysiology. This review introduces recent evidence of GSNO-mediated NO/SNO signaling depending on GSNOR expression or activity. In addition, the applicability of GSNOR as a target for drug therapy will be discussed in this review.

• Proceedings of the Microbiological Society of Korea Conference
• /
• 2002.10a
• /
• pp.219.1-219.1
• /
• 2002

• Proceedings of the Korean Society of Life Science Conference
• /
• 2007.10a
• /
• pp.91.1-91.1
• /
• 2007

See Full Text

• Korean Journal of Microbiology
• /
• v.38 no.4
• /
• pp.260-266
• /
• 2002

In this study, chromosomal DNA fragment related to the regulation of phenol metabolism in Ralstonia eutropha JMP 134 was cloned and sequenced. The result has shown that two open reading frames (ORF1 and ORF2) exist on this regulatory region. ORF1, which initiates from 454 bp downstream of the stop codon of the phenol hydroxylase genes, was found to be composed of 501 amino acids. ORF2, whose start codon is overlapped with the stop codon of ORFl, was found to contain 232 amino acids. The comparison of amino acid sequences with other proteins has revealed that ORF1 belongs to the family of NtrC transcriptional activator, whereas ORF2 shares high homology with the family of GntR protein, which is known to be a negative regulator. ORF1 and ORF2 were designated as a putative positive regulator, phlR2 and a negative regulator phlA, respectively. Possible regulatory mechanisms of phenol metabolism in this strain was discussed.

• Proceedings of the Korean Biophysical Society Conference
• /
• 2003.06a
• /
• pp.50-50
• /
• 2003

We have identified and analysed a putative response regulator two-component gene (CaSKN7) from Candida albicans and its encoding protein (CaSkn7). CaSKN7 has an open reading frame of 1677bp. CaSKN7 encodes a 559 amino acid protein (CaSkn7) with an estimated molecular mass of 61.1 kDa. CaSKN7 is a homologue of a Saccharomyces cerevisiae SKN7 that is the regulator involved in the oxidative stress response. To study the role of CaSKN7, we constructed a CAI4-derived mutant strain carrying a homozygous deletion of the CaSKN7 gene. In the caskn7 disruptant cells, the formation of germ tube require shorter time than that in the congenic wild-type strain but the growth of mycelium delayed in liquid media. In contrast, the caskn7 disruptant cells attenuate the differentiation in solid media and the virulence in mouse model system. Expression level of hypha-specific and virulence genes - HYR1, ECE1, HWP1, and ALS1 - in the caskn7 disruptant cells increased as compared with that in the congenic wild-type strain in 10％ serum YPD. Skn7 in 5. cerevisiae was found to bind the HSE element from the SSA promoter, Also, CaSkn7 contains heat shock factor DNA-binding domain and the promoters of these genes have HSE-like sties. Therefore these results show that CaSKN7 regulate the differentiation and virulence of C. albicans.

• BMB Reports
• /
• v.54 no.3
• /
• pp.164-169
• /
• 2021

Neuronal growth regulator 1 (NEGR1) is a GPI-anchored membrane protein that is involved in neural cell adhesion and communication. Multiple genome wide association studies have found that NEGR1 is a generic risk factor for multiple human diseases, including obesity, autism, and depression. Recently, we reported that Negr1-/- mice showed a highly increased fat mass and affective behavior. In the present study, we identified Na/K-ATPase, beta1-subunit (ATP1B1) as an NEGR1 binding partner by yeast two-hybrid screening. NEGR1 and ATP1B1 were found to form a relatively stable complex in cells, at least partially co-localizing in membrane lipid rafts. We found that NEGR1 binds with ATP1B1 at its C-terminus, away from the binding site for the alpha subunit, and may contribute to intercellular interactions. Collectively, we report ATP1B1 as a novel NEGR1-interacting protein, which may help deciphering molecular networks underlying NEGR1-associated human diseases.

• International Journal of Stem Cells
• /
• v.16 no.4
• /
• pp.394-405
• /
• 2023

The differentiation of pluripotent stem cells has been used to study disease mechanisms and development. We previously described a method for differentiating human pluripotent stem cells (hPSCs) into salivary gland epithelial progenitors (SGEPs). Here, cystic fibrosis transmembrane conductance regulator (CFTR) knockout hPSCs were differentiated into SGEPs derived from CFTR knockout hESCs (CF-SGEPs) using the same protocol to investigate whether the hPSC-derived SGEPs can model the characteristics of CF. CF-a disease that affects salivary gland (SG) function-is caused by mutations of the CFTR gene. Firstly, we successfully generated CFTR knockout hPSCs with reduced CFTR protein expression using the CRISPR-Cas9 system. After 16 days of differentiation, the protein expression of CFTR decreased in SGEPs derived from CFTR knockout hESCs (CF-SGEPs). RNA-Seq revealed that multiple genes modulating SG development and function were down-regulated, and positive regulators of inflammation were up-regulated in CF-SGEPs, correlating with the salivary phenotype of CF patients. These results demonstrated that CFTR suppression disrupted the differentiation of hPSC-derived SGEPs, which modeled the SG development of CF patients. In summary, this study not only proved that the hPSC-derived SGEPs could serve as manipulable and readily accessible cell models for the study of SG developmental diseases but also opened up new avenues for the study of the CF mechanism.

• Journal of the Korean Magnetic Resonance Society
• /
• v.17 no.1
• /
• pp.59-66
• /
• 2013

BldD, a developmental transcription factor from Streptomyces coelicolor, is a homodimeric, DNA-binding protein with 167 amino acids in each subunit. Each monomer consists of two structurally distinct domains, the N-terminal domain (BldD-NTD) responsible for DNA-binding and dimerization and the C-terminal domain (BldD-CTD). In contrast to the BldD-NTD, of which crystal structure has been solved, the BldD-CTD has been characterized neither in structure nor in function. Thus, in terms of structural genomics, structural study of the BldD-CTD has been conducted in solution, and in the present work, mainchain NMR assignments of the recombinant BldD-CTD (residues 80-167 of BldD) could be achieved by a series of heteronuclear multidimensional NMR experiments on a [$^{13}C/^{15}N$]-enriched protein sample. Finally, the secondary structure prediction by CSI and TALOS+ analysis using the assigned chemical shifts data identified a ${\beta}-{\alpha}-{\alpha}-{\beta}-{\alpha}-{\alpha}-{\alpha}$ topology of the domain. The results will provide the most fundamental data for more detailed approach to the atomic structure of the BldD-CTD, which would be essential for entire understanding of the molecular function of BldD.

• BMB Reports
• /
• v.51 no.5
• /
• pp.207-208
• /
• 2018

Chitinase-Like Proteins (CLPs) are an evolutionarily conserved protein which lose their enzymatic activity for degrading chitin macromolecules. Chitinase-3-like-1 (Chi3l1) is a type of CLP that is highly expressed in epithelial cells, macrophages, etc., and is known to have correlations with type 2 inflammation and cancer. Although the increased level of Chi3l1 in the blood was reported in various disease patients, the function of Chi3l1 in adaptive immunity has been totally unknown. Recently, we found that Chi3l1 is expressed in T cells and has a negative regulatory role in T-cell activation and proliferation. A genetic ablation study of Chi3l1 in T cells showed hyperresponsiveness to TcR stimulation, which increased proliferation and Th1 differentiation. A significant increase of $IFN{\gamma}$ signaling in Chi3l1-deficient T cells synergistically increased Th1 and CTL functions against melanoma cells in vitro and in vivo. In addition, targeted knockdown by Chi3l1 siRNA complexed with the cell-penetrating peptide dNP2, which showed decreased pulmonary melanoma metastasis with increased infiltration of Th1 and CTL in the lung. This study first suggests that Chi3l1 is a novel regulator of Th1/CTL responses and could be a target for treating cancer to increase tumor immunity.