간행물

BMB Reports update

Biochemistry and Molecular Biology Reports

  • : 생화학분자생물학회
  • : 자연과학분야  >  화학
  • : KCI등재
  • : SCOPUS
  • : 연속간행물
  • : 월간
  • : 1976-6696
  • : 1976-670X
  • : Korean Biochemical Journal(~1994)→Journal of Biochemistry and Molecular Biology(1995~)→Biochemistry and Molecurar Biology Reports(2008~)

수록정보
수록범위 : 1권1호(1968)~55권8호(2022) |수록논문 수 : 4,617
BMB Reports
55권8호(2022년 08월) 수록논문
최근 권호 논문
| | | |

KCI등재 SCOPUS

저자 : Chan-geun Kim , Da-eun Hwang , Rajeev Kumar , Min Chung , Yu-gon Eom , Hyunji Kim , Da-hyun Koo , Jeong-mo Choi

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 8호 발행 연도 : 2022 페이지 : pp. 364-370 (7 pages)

다운로드

(기관인증 필요)

초록보기

Biomolecular phase separation has recently attracted broad interest, due to its role in the spatiotemporal compartmentalization of living cells. It governs the formation, regulation, and dissociation of biomolecular condensates, which play multiple roles in vivo, from activating specific biochemical reactions to organizing chromatin. Interestingly, biomolecular phase separation seems to be a mainly passive process, which can be explained by relatively simple physical principles and reproduced in vitro with a minimal set of components. This Mini review focuses on our current understanding of the fundamental principles of biomolecular phase separation and the recent progress in the research on this topic. [BMB Reports 2022; 55(8): 363-369]

KCI등재 SCOPUS

저자 : Ramkumar Menon

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 8호 발행 연도 : 2022 페이지 : pp. 370-379 (10 pages)

다운로드

(기관인증 필요)

초록보기

Human pregnancy is a delicate and complex process where multiorgan interactions between two independent systems, the mother, and her fetus, maintain pregnancy. Intercellular interactions that can define homeostasis at the various cellular level between the two systems allow uninterrupted fetal growth and development until delivery. Interactions are needed for tissue remodeling during pregnancy at both fetal and maternal tissue layers. One of the mechanisms that help tissue remodeling is via cellular transitions where epithelial cells undergo a cyclic transition from epithelial to mesenchymal (EMT) and back from mesenchymal to epithelial (MET). Two major pregnancy-associated tissue systems that use EMT, and MET are the fetal membrane (amniochorion) amnion epithelial layer and cervical epithelial cells and will be reviewed here. EMT is often associated with localized inflammation, and it is a well-balanced process to facilitate tissue remodeling. Cyclic transition processes are important because a terminal state or the static state of EMT can cause accumulation of proinflammatory mesenchymal cells in the matrix regions of these tissues and increase localized inflammation that can cause tissue damage. Interactions that determine homeostasis are often controlled by both endocrine and paracrine mediators. Pregnancy maintenance hormone progesterone and its receptors are critical for maintaining the balance between EMT and MET. Increased intrauterine oxidative stress at term can force a static (terminal) EMT and increase inflammation that are physiologic processes that destabilize homeostasis that maintain pregnancy to promote labor and delivery of the fetus. However, conditions that can produce an untimely increase in EMT and inflammation can be pathologic. These tissue damages are often associated with adverse pregnancy complications such as preterm prelabor rupture of the membranes (pPROM) and spontaneous preterm birth (PTB). Therefore, an understanding of the biomolecular processes that maintain cyclic EMT-MET is critical to reducing the risk of pPROM and PTB. Extracellular vesicles (exosomes of 40-160 nm) that can carry various cargo are involved in cellular transitions as paracrine mediators. Exosomes can carry a variety of biomolecules as cargo. Studies specifically using exosomes from cells undergone EMT can carry a pro-inflammatory cargo and in a paracrine fashion can modify the neighboring tissue environment to cause enhancement of uterine inflammation. [BMB Reports 2022; 55(8): 370-379]

KCI등재 SCOPUS

저자 : Sang Hyeon Kim , In Ryeong Jung , Soo Seok Hwang

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 8호 발행 연도 : 2022 페이지 : pp. 380-388 (9 pages)

다운로드

(기관인증 필요)

초록보기

The B cell translocation gene 1 (BTG1) and BTG2 play a key role in a wide range of cellular activities including proliferation, apoptosis, and cell growth via modulating a variety of central biological steps such as transcription, post-transcriptional, and translation. BTG1 and BTG2 have been identified by genomic profiling of B-cell leukemia and diverse lymphoma types where both genes are commonly mutated, implying that they serve as tumor suppressors. Furthermore, a low expression level of BTG1 or BTG2 in solid tumors is frequently associated with malignant progression and poor treatment outcomes. As physiological aspects, BTG1 and BTG2 have been discovered to play a critical function in regulating quiescence in hematopoietic lineage such as Hematopoietic stem cells (HSCs) and naïve and memory T cells, highlighting their novel role in maintaining the quiescent state. Taken together, emerging evidence from the recent studies suggests that BTG1 and BTG2 play a central anti-proliferative role in various tissues and cells, indicating their potential as targets for innovative therapeutics. [BMB Reports 2022; 55(8): 380-388]

KCI등재 SCOPUS

저자 : Nur Aziz , Eunji Kim , Yanyan Yang , Han Gyung Kim , Tao Yu , Jae Youl Cho

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 8호 발행 연도 : 2022 페이지 : pp. 389-394 (6 pages)

다운로드

(기관인증 필요)

초록보기

In particular, the phenomenon of c-Jun degradation within the inflammatory response has not yet been fully analyzed. In order to verify this, we investigated LPS-stimulated murine macrophages pre-treated with sodium orthovanadate (SO) in order to uncover the regulatory mechanisms of the MAPKs which regulate c-Jun degradation within the inflammatory response. Through our study, we found that SO suppressed the production of prostaglandin E2 (PGE2) and the expression of COX-2 in LPS-stimulated RAW264.7 cells. Additionally, SO decreased total c-Jun levels, without altering the amount of mRNA, although the phospho-levels of p38, ERK, and JNK were strongly enhanced. Through the usage of selective MAPK inhibitors, and knockdown and overexpression strategies, p38 was revealed to be a major MAPK which regulates c-Jun degradation. Further analysis indicates that the phosphorylation of p38 is a determinant for c-Jun degradation, and is sufficient to induce ubiquitination-dependent c-Jun degradation, recovered through MG132 treatment. Therefore, our results suggest that the hyperphosphorylation of p38 by SO contributes to c-Jun degradation, which is linked to the suppression of PGE2 secretion in inflammatory responses; and thus, finding drugs to increase p38 activity could be a novel strategy for the development of anti-inflammatory drugs. [BMB Reports 2022; 55(8): 389-394]

KCI등재 SCOPUS

저자 : Yu Sun Jeong , Sunghyun Huh , Ji Cheol Kim , Ji Ye Park , Chaeeun Lee , Min-sik Kim , Jaehyung Koo , Yoe-sik Bae

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 8호 발행 연도 : 2022 페이지 : pp. 395-400 (6 pages)

다운로드

(기관인증 필요)

초록보기

Pseudomonas aeruginosa (P. aeruginosa) is a well-known Gramnegative opportunistic pathogen. Neutrophils play key roles in mediating host defense against P. aeruginosa infection. In this study, we identified a metabolite derived from P. aeruginosa that regulates neutrophil activities. Using gas chromatography-mass spectrometry, a markedly increased level of 2-undecanone was identified in the peritoneal fluid of P. aeruginosa-infected mice. 2-Undecanone elicited the activation of neutrophils in a Gαi-phospholipase C pathway. However, 2-undecanone strongly inhibited responses to lipopolysaccharide and bactericidal activity of neutrophils against P. aeruginosa by inducing apoptosis. Our results demonstrate that 2-undecanone from P. aeruginosa limits the innate defense activity of neutrophils, suggesting that the production of inhibitory metabolites is a strategy of P. aeruginosa for escaping the host immune system. [BMB Reports 2022; 55(8): 395-400]

KCI등재 SCOPUS

저자 : Insook Yang , Yeri Son , Jae Hoon Shin , Il Yong Kim , Je Kyung Seong

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 8호 발행 연도 : 2022 페이지 : pp. 401-406 (6 pages)

다운로드

(기관인증 필요)

초록보기

Ahnak, a large protein first identified as an inhibitor of TGF-β signaling in human neuroblastoma, was recently shown to promote TGF-β in some cancers. The TGF-β signaling pathway regulates cell growth, various biological functions, and cancer growth and metastasis. In this study, we used Ahnak knockout (KO) mice that underwent a 70% partial hepatectomy (PH) to investigate the function of Ahnak in TGF-β signaling during liver regeneration. At the indicated time points after PH, we analyzed the mRNA and protein expression of the TGF -β/Smad signaling pathway and cell cycle-related factors, evaluated the cell cycle through proliferating cell nuclear antigen (PCNA) immunostaining, analyzed the mitotic index by hematoxylin and eosin staining. We also measured the ratio of liver tissue weight to body weight. Activation of TGF-β signaling was confirmed by analyzing the levels of phospho-Smad 2 and 3 in the liver at the indicated time points after PH and was lower in Ahnak KO mice than in WT mice. The expression levels of cyclin B1, D1, and E1; proteins in the Rb/E2F transcriptional pathway, which regulates the cell cycle; and the numbers of PCNA-positive cells were increased in Ahnak KO mice and showed tendencies opposite that of TGF-β expression. During postoperative regeneration, the liver weight to body weight ratio tended to increase faster in Ahnak KO mice. However, 7 days after PH, both groups of mice showed similar rates of regeneration, following which their active regeneration stopped. Analysis of hepatocytes undergoing mitosis showed that there were more mitotic cells in Ahnak KO mice, consistent with the weight ratio. Our findings suggest that Ahnak enhances TGF-β signaling during postoperative liver regeneration, resulting in cell cycle disruption; this highlights a novel role of Ahnak in liver regeneration. These results provide new insight into liver regeneration and potential treatment targets for liver diseases that require surgical treatment. [BMB Reports 2022; 55(8): 401-406]

KCI등재 SCOPUS

저자 : Bo-sung Kim , Minwook Shin , Kyu-won Kim , Ki-tae Ha , Sung-jin Bae

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 55권 8호 발행 연도 : 2022 페이지 : pp. 407-412 (6 pages)

다운로드

(기관인증 필요)

초록보기

A well-controlled inflammatory response is crucial for the recovery from injury and maintenance of tissue homeostasis. The anti-inflammatory response of 2-methoxycinnamaldehyde (2-MCA), a natural compound derived from cinnamon, has been studied; however, the underlying mechanism on macrophage has not been fully elucidated. In this study, LPS-stimulated production of TNF-α and NO was reduced by 2-MCA in macrophages. 2-MCA significantly activated the NRF2 pathway, and expression levels of autophagy-associated proteins in macrophages, including LC3 and P62, were enhanced via NRF2 activation regardless of LPS treatment, suggesting the occurrence of 2-MCA-mediated autophagy. Moreover, evaluation of autophagy flux using luciferase-conjugated LC3 revealed that incremental LC3 and P62 levels are coupled to enhanced autophagy flux. Finally, reduced expression levels of TNF-α and NOS2 by 2-MCA were reversed by autophagy inhibitors, such as bafilomycin A1 and NH4Cl, in LPS-stimulated macrophages. In conclusion, 2-MCA enhances autophagy flux in macrophages via NRF2 activation and consequently reduces LPS-induced inflammation. [BMB Reports 2022; 55(8): 407-412]

1
권호별 보기

내가 찾은 최근 검색어

최근 열람 자료

맞춤 논문

보관함

내 보관함
공유한 보관함

1:1문의

닫기