Journal of biochemistry最新文献_第10页

C-terminal truncation is a prominent post-translational modification of human erythrocyte α-synuclein. C端截短是人类红细胞α-突触核蛋白的一种显著的翻译后修饰。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-05-31 DOI: 10.1093/jb/mvae012

Ryosuke Amagai, Riki Otomo, Sakura Yoshioka, Hidekazu Nagano, Naoko Hashimoto, Ryuji Sakakibara, Tomoaki Tanaka, Ayako Okado-Matsumoto

{"title":"C-terminal truncation is a prominent post-translational modification of human erythrocyte α-synuclein.","authors":"Ryosuke Amagai, Riki Otomo, Sakura Yoshioka, Hidekazu Nagano, Naoko Hashimoto, Ryuji Sakakibara, Tomoaki Tanaka, Ayako Okado-Matsumoto","doi":"10.1093/jb/mvae012","DOIUrl":"10.1093/jb/mvae012","url":null,"abstract":"α-Synuclein (α-Syn) is a protein related to synucleinopathies with high expression in the central nervous system and erythrocytes which are a major source of peripheral α-Syn. Recent reports have suggested the presence of α-Syn within extracellular vesicles (EVs) derived from erythrocytes, potentially contributing to the pathogenesis of synucleinopathies. While Lewy bodies, intracellular inclusions containing aggregated α-Syn, are prominently observed within the brain, their occurrence in peripheral neurons implies the dissemination of synucleinopathy pathology throughout the body via the propagation of α-Syn. In this study, we found erythrocytes and circulating EVs obtained from plasma contained α-Syn, which was separated into four major forms using high-resolution clear native-PAGE and isoelectric focusing. Notably, erythrocyte α-Syn was classified into full-length and C-terminal truncated forms, with truncation observed between Y133 and Q134 as determined by LC-MS/MS analysis. Our finding revealed that C-terminally truncated α-Syn, which was previously reported to exist solely within the brain, was also present in erythrocytes and circulating EVs obtained from plasma.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"649-658"},"PeriodicalIF":2.1,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139671893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Extracellular histones promote calcium phosphate-dependent calcification in mouse vascular smooth muscle cells. 细胞外组蛋白促进小鼠血管平滑肌细胞中磷酸钙依赖性钙化

IF 2.7 4区生物学

Journal of biochemistry Pub Date : 2024-05-31 DOI: 10.1093/jb/mvae011

Tomonori Hoshino, Davood Kharaghani, Shohei Kohno

{"title":"Extracellular histones promote calcium phosphate-dependent calcification in mouse vascular smooth muscle cells.","authors":"Tomonori Hoshino, Davood Kharaghani, Shohei Kohno","doi":"10.1093/jb/mvae011","DOIUrl":"10.1093/jb/mvae011","url":null,"abstract":"Vascular calcification, a major risk factor for cardiovascular events, is associated with a poor prognosis in chronic kidney disease (CKD) patients. This process is often associated with the transformation of vascular smooth muscle cells (VSMCs) into cells with osteoblast-like characteristics. Damage-associated molecular patterns (DAMPs), such as extracellular histones released from damaged or dying cells, are suspected to accumulate at calcification sites. To investigate the potential involvement of DAMPs in vascular calcification, we assessed the impact of externally added histones (extracellular histones) on calcium and inorganic phosphate-induced calcification in mouse VSMCs. Our study found that extracellular histones intensified calcification. We also observed that the histones decreased the expression of VSMC marker genes while simultaneously increasing the expression of osteoblast marker genes. Additionally, histones treated with DNase I, which degrades dsDNA, attenuated this calcification, compared with the non-treated histones, suggesting a potential involvement of dsDNA in this process. Elevated levels of dsDNA were also detected in the serum of CKD model mice, underlining its potential role in vascular calcification in CKD. Our findings suggest that extracellular histones could play a pivotal role in the vascular calcification observed in CKD.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"643-648"},"PeriodicalIF":2.7,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139671894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular structure and function of mysterin/RNF213. 神秘蛋白/RNF213的分子结构和功能。

IF 2.7 4区生物学

Journal of biochemistry Pub Date : 2024-04-29 DOI: 10.1093/jb/mvae020

Daisuke Morito

{"title":"Molecular structure and function of mysterin/RNF213.","authors":"Daisuke Morito","doi":"10.1093/jb/mvae020","DOIUrl":"10.1093/jb/mvae020","url":null,"abstract":"Mysterin is a large intracellular protein harboring a RING finger ubiquitin ligase domain and is also referred to as RING finger protein 213 (RNF213). The author performed the first molecular cloning of the mysterin gene as the final step in genetic exploration of cerebrovascular moyamoya disease (MMD) and initiated the next round of exploration to understand its molecular and cellular functions. Although much remains unknown, accumulating findings suggest that mysterin functions in cells by targeting massive intracellular structures, such as lipid droplets (LDs) and various invasive pathogens. In the latter case, mysterin appears to directly surround and ubiquitylate the surface of pathogens and stimulate cell-autonomous antimicrobial reactions, such as xenophagy and inflammatory response. To date, multiple mutations causing MMD have been identified within and near the RING finger domain of mysterin; however, their functional relevance remains largely unknown. Besides the RING finger, mysterin harbors a dynein-like ATPase core and an RZ finger, another ubiquitin ligase domain unique to mysterin, while functional exploration of these domains has also just commenced. In this review, the author attempts to summarize the core findings regarding the molecular structure and function of the mysterin protein, with an emphasis on the perspective of MMD research.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"495-505"},"PeriodicalIF":2.7,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139912677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Perturbed collagen metabolism underlies lymphatic recanalization failure in Gata2 heterozygous deficient mice. 胶原代谢紊乱是 Gata2 杂合子缺陷小鼠淋巴再闭合失败的原因。

IF 2.7 4区生物学

Journal of biochemistry Pub Date : 2024-04-29 DOI: 10.1093/jb/mvad122

Tomomi Watanabe-Asaka, Moyuru Hayashi, Takuya Harada, Satoshi Uemura, Jun Takai, Yasuhiro Nakamura, Takashi Moriguchi, Yoshiko Kawai

{"title":"Perturbed collagen metabolism underlies lymphatic recanalization failure in Gata2 heterozygous deficient mice.","authors":"Tomomi Watanabe-Asaka, Moyuru Hayashi, Takuya Harada, Satoshi Uemura, Jun Takai, Yasuhiro Nakamura, Takashi Moriguchi, Yoshiko Kawai","doi":"10.1093/jb/mvad122","DOIUrl":"10.1093/jb/mvad122","url":null,"abstract":"Lymphedema has become a global health issue following the growing number of cancer surgeries. Curative or supportive therapeutics have long been awaited for this refractory condition. Transcription factor GATA2 is crucial in lymphatic development and maintenance, as GATA2 haploinsufficient disease often manifests as lymphedema. We recently demonstrated that Gata2 heterozygous deficient mice displayed delayed lymphatic recanalization upon lymph node resection. However, whether GATA2 contributes to lymphatic regeneration by functioning in the damaged lymph vessels' microenvironment remains explored. In this study, our integrated analysis demonstrated that dermal collagen fibers were more densely accumulated in the Gata2 heterozygous deficient mice. The collagen metabolism-related transcriptome was perturbed, and collagen matrix contractile activity was aberrantly increased in Gata2 heterozygous embryonic fibroblasts. Notably, soluble collagen placement ameliorated delayed lymphatic recanalization, presumably by modulating the stiffness of the extracellular matrix around the resection site of Gata2 heterozygous deficient mice. Our results provide valuable insights into mechanisms underlying GATA2-haploinsufficiency-mediated lymphedema and shed light on potential therapeutic avenues for this intractable disease.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"551-560"},"PeriodicalIF":2.7,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139087013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

On the pursuit to reconstitute the Escherichia coli ribosome from purified components. 关于利用纯化成分重组大肠杆菌核糖体的研究。

IF 2.7 4区生物学

Journal of biochemistry Pub Date : 2024-04-29 DOI: 10.1093/jb/mvad121

Hideki Taguchi

引用次数: 0

Protein degraders - from thalidomide to new PROTACs. 蛋白质降解剂--从沙利度胺到新的 PROTACs。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-04-29 DOI: 10.1093/jb/mvad113

Takumi Ito

{"title":"Protein degraders - from thalidomide to new PROTACs.","authors":"Takumi Ito","doi":"10.1093/jb/mvad113","DOIUrl":"10.1093/jb/mvad113","url":null,"abstract":"Recently, the development of protein degraders (protein-degrading compounds) has prominently progressed. There are two remarkable classes of protein degraders: proteolysis-targeting chimeras (PROTACs) and molecular glue degraders (MGDs). Almost 70 years have passed since thalidomide was initially developed as a sedative-hypnotic drug, which is currently recognized as one of the most well-known MGDs. During the last two decades, a myriad of PROTACs and MGDs have been developed, and the molecular mechanism of action (MOA) of thalidomide was basically elucidated, including identifying its molecular target cereblon (CRBN). CRBN forms a Cullin Ring Ligase 4 with Cul4 and DDB1, whose substrate specificity is controlled by its binding ligands. Thalidomide, lenalidomide and pomalidomide, three CRBN-binding MGDs, were clinically approved to treat several intractable diseases (including multiple myeloma). Several other MGDs and CRBN-based PROTACs (ARV-110 and AVR-471) are undergoing clinical trials. In addition, several new related technologies regarding PROTACs and MGDs have also been developed, and achievements of protein degraders impact not only therapeutic fields but also basic biological science. In this article, I introduce the history of protein degraders, from the development of thalidomide to the latest PROTACs and related technologies.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"507-519"},"PeriodicalIF":2.1,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138885083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to: The Largest Subunit of Human TFIIIC Complex, TFIIIC220, a Lysine Acetyltransferase Targets Histone H3K18. 更正：人类 TFIIIC 复合物的最大亚基 TFIIIC220 是一种靶向组蛋白 H3K18 的赖氨酸乙酰转移酶。

IF 2.7 4区生物学

Journal of biochemistry Pub Date : 2024-04-29 DOI: 10.1093/jb/mvae025

引用次数: 0

Notch signaling pathway induces expression of type IV collagen in angiogenesis. Notch 信号通路在血管生成过程中诱导 IV 型胶原蛋白的表达。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-04-29 DOI: 10.1093/jb/mvad120

Kazuki Kukita, Nanaka Matsuzaka, Mikihisa Takai, Yasutada Imamura, Yongchol Shin

{"title":"Notch signaling pathway induces expression of type IV collagen in angiogenesis.","authors":"Kazuki Kukita, Nanaka Matsuzaka, Mikihisa Takai, Yasutada Imamura, Yongchol Shin","doi":"10.1093/jb/mvad120","DOIUrl":"10.1093/jb/mvad120","url":null,"abstract":"Mural cell adhesion is important for the localization of basement membrane components during angiogenesis, and cell-cell interactions are thought to be critical for basement membrane formation. Type IV collagen, a component of the basement membrane, and non-triple helical type IV collagen α1 chain (NTH α1(IV)) co-localize in the basement membrane of neovascular vessels. However, it remains unclear how type IV collagen and NTH α1(IV) are produced around the basement membrane. In the present study, we developed a de novo angiogenesis model using human umbilical vein endothelial cell spheroids and TIG-1 fibroblast cells and demonstrated that NTH α1(IV), probably with α1(IV) chain before forming triple helix molecule, was localized in the fibroblasts in contact with vascular endothelial cells. This localization was disrupted by DAPT, a Notch signaling inhibitor. DAPT treatment also reduced type IV collagen and NTH α1(IV) secretion in TIG-1 fibroblasts, along with diminished COL4A1 and COL4A2 gene expression. Downregulation of Notch3 in TIG-1 fibroblasts decreased the secretion of type IV collagen and NTH α1(IV). Taken together, these findings suggest that heterogeneous and homogeneous intercellular Notch signaling via Notch3 induces type IV collagen and NTH α1(IV) expression in fibroblasts and contributes to basement membrane formation in neovascular vessels.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"539-549"},"PeriodicalIF":2.1,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139087012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Therapeutic strategies targeting cellular senescence for cancer and other diseases. 针对癌症和其他疾病的细胞衰老治疗策略。

IF 2.7 4区生物学

Journal of biochemistry Pub Date : 2024-04-29 DOI: 10.1093/jb/mvae015

Xuebing Wang, Takeshi Fukumoto, Ken-Ichi Noma

引用次数: 0

Protein homeostasis and degradation in quiescent neural stem cells. 静止神经干细胞的蛋白质平衡与降解

IF 2.7 4区生物学

Journal of biochemistry Pub Date : 2024-04-29 DOI: 10.1093/jb/mvae006

Taeko Kobayashi

{"title":"Protein homeostasis and degradation in quiescent neural stem cells.","authors":"Taeko Kobayashi","doi":"10.1093/jb/mvae006","DOIUrl":"10.1093/jb/mvae006","url":null,"abstract":"Tissue stem cells are maintained in the adult body throughout life and are crucial for tissue homeostasis as they supply newly functional cells. Quiescence is a reversible arrest in the G0/G1 phase of the cell cycle and a strategy to maintain the quality of tissue stem cells. Quiescence maintains stem cells in a self-renewable and differentiable state for a prolonged period by suppressing energy consumption and cell damage and depletion. Most adult neural stem cells in the brain maintain the quiescent state and produce neurons and glial cells through differentiation after activating from the quiescent state to the proliferating state. In this process, proteostasis, including proteolysis, is essential to transition between the quiescent and proliferating states associated with proteome remodeling. Recent reports have demonstrated that quiescent and proliferating neural stem cells have different expression patterns and roles as proteostatic molecules and are affected by age, indicating differing processes for protein homeostasis in these two states in the brain. This review discusses the multiple regulatory stages from protein synthesis (protein birth) to proteolysis (protein death) in quiescent neural stem cells.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"481-486"},"PeriodicalIF":2.7,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139650827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0