Journal of biochemistry最新文献

Transcription and translation efficiency is reduced in cholesterol-containing liposomes. 在含胆固醇的脂质体中，转录和翻译效率降低。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-06-13 DOI: 10.1093/jb/mvaf032

Shota Fukuoka, Ayu Shimomura, Yuya Katsumura, Masaya Oki, Gakushi Tsuji

引用次数: 0

Bisecting GlcNAc modification of angiotensin-related glycoproteins in mouse kidney. GlcNAc对小鼠肾脏血管紧张素相关糖蛋白的修饰。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-06-13 DOI: 10.1093/jb/mvaf033

Haruka Kawade, Wanxue Bao, Yuko Tokoro, Yoshimasa Ito, Yudai Tsuji, Kazuo Takahashi, Kazuki Nakajima, Miyako Nakano, Yasuhiko Kizuka

{"title":"Bisecting GlcNAc modification of angiotensin-related glycoproteins in mouse kidney.","authors":"Haruka Kawade, Wanxue Bao, Yuko Tokoro, Yoshimasa Ito, Yudai Tsuji, Kazuo Takahashi, Kazuki Nakajima, Miyako Nakano, Yasuhiko Kizuka","doi":"10.1093/jb/mvaf033","DOIUrl":"https://doi.org/10.1093/jb/mvaf033","url":null,"abstract":"Structural variations of N-glycans critically regulate glycoprotein functions and are involved in various human diseases. N-Acetylglucosaminyltransferase-III (GnT-III or MGAT3) is highly expressed in the brain and kidney and is an N-glycan branching enzyme that biosynthesizes the unique N-glycan branch designated as bisecting GlcNAc. Its roles in Alzheimer's disease and cancer have been revealed, but the functions of bisecting GlcNAc in the kidney are poorly understood. Here, we show that kidneys in the GnT-III-knockout (KO) mouse exhibit impaired body fluid balance and present interstitial edema. To understand the molecular mechanisms further, we biochemically purified the glycoproteins modified by GnT-III in the mouse kidney and identified these proteins using proteomics. We found that the proteins involved in the pathway for angiotensin II (Ang II) metabolism are modified by GnT-III, and that the subcellular localization of angiotensin converting enzyme was altered in GnT-III-KO cells. Furthermore, the pathology in models of Ang II-related disease was slightly more severe in GnT-III-KO than in wild-type mice. Our data indicate a protective role for bisecting GlcNAc in the mouse kidney, highlighting a newly described link between specific N-glycan structures and renal functions.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284438","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

Differential regulation between photosynthetic type and non-photosynthetic type Fd:FNRs in the negative cooperativity and pH dependency of the electron transfer activity. 光合型与非光合型FNRs对电子转移活性负协同性和pH依赖性的差异调控。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-06-10 DOI: 10.1093/jb/mvaf031

Yoko Kimata-Ariga, Shunsuke Miyake, Takato Murakami, Shunsuke Kuwano

{"title":"Differential regulation between photosynthetic type and non-photosynthetic type Fd:FNRs in the negative cooperativity and pH dependency of the electron transfer activity.","authors":"Yoko Kimata-Ariga, Shunsuke Miyake, Takato Murakami, Shunsuke Kuwano","doi":"10.1093/jb/mvaf031","DOIUrl":"https://doi.org/10.1093/jb/mvaf031","url":null,"abstract":"In higher plants, ferredoxin (Fd) and Fd-NADP+ reductase (FNR) are each present as distinct isoproteins of photosynthetic type and non-photosynthetic type, which exhibit differential function despite their similarity in the 3D structures. In this study, we addressed differential regulation of Fd/FNR reaction between the two types from two perspectives and investigated the amino acid residues of Fd responsible for the differences. Firstly, pH-dependent profile of Fd/FNR electron transfer activity varied among the combinations of the two types of Fd and FNR; non-photosynthetic type FNR showed similar pattern for the two types of Fds while photosynthetic type FNR was previously shown to exhibit opposite pattern which was explained by the different pH-dependent profile of Km for the two Fds. Secondly, the extent of the suppression of the affinity (in terms of Km value) between Fd and FNR by NADPH significantly varied among the combinations of the two types of Fd:FNR. The difference was shown to be mainly due to the different property of Fd between the two types. Kinetic analyses using site-directed mutants of Fd showed the contribution of C-terminal residues, together with that of 78th residue of Fd, on the differential profile of Fd/FNR reaction by pH and NADPH.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258162","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

Three glutamic acid residues in the cytoplasmic N-terminal tail of long-form GlcAT-P define Golgi-to-ER trafficking. 长形GlcAT-P的细胞质n端尾部的三个谷氨酸残基定义了高尔基到内质网的运输。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-06-09 DOI: 10.1093/jb/mvaf030

Ayaka Okada, Risa Harui, Tomonari Ishida, Katsuaki Higashi, Motohiro Nonaka, Shogo Oka, Jyoji Morise

{"title":"Three glutamic acid residues in the cytoplasmic N-terminal tail of long-form GlcAT-P define Golgi-to-ER trafficking.","authors":"Ayaka Okada, Risa Harui, Tomonari Ishida, Katsuaki Higashi, Motohiro Nonaka, Shogo Oka, Jyoji Morise","doi":"10.1093/jb/mvaf030","DOIUrl":"https://doi.org/10.1093/jb/mvaf030","url":null,"abstract":"Glucuronyltransferase GlcAT-P is a rate-limiting enzyme involved in the biosynthesis of the Human Natural Killer-1 carbohydrate and is essential for acquiring higher brain functions. Alternative splicing produces two isoforms, short-form GlcAT-P (sGlcAT-P) and long-form GlcAT-P (lGlcAT-P), which share identical peptide sequences except for an additional 13 amino acids (AA) in the cytoplasmic N-terminal tail of lGlcAT-P. Although sGlcAT-P localizes to the Golgi apparatus (GA), where many glycosyltransferases reside, lGlcAT-P is distributed in both the GA and endoplasmic reticulum (ER). However, the mechanisms responsible for this distinct intracellular distribution remain poorly understood. In this study, we explored the role of the 13 AA in the cytoplasmic N-tail of lGlcAT-P in trafficking between the GA and the ER using the Retention Using Selective Hooks system. Our findings revealed that lGlcAT-P undergoes enhanced retrograde trafficking from the GA to the ER, whereas its anterograde trafficking from the ER to the GA remains largely unaffected. In addition, three glutamic acid residues within the 13 AA of lGlcAT-P were identified as crucial for promoting retrograde trafficking. These results suggest that the ER distribution of lGlcAT-P is primarily governed by Golgi-to-ER trafficking regulated by specific sequences in its cytoplasmic N-tail.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248033","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

Acquisition mechanism of heme oxygenase-1 induction by heat shock in human monocytic cell line THP-1 after differentiation to macrophage-like cells. 热休克诱导单核细胞THP-1向巨噬细胞样细胞分化后血红素氧合酶-1的获取机制

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-05-30 DOI: 10.1093/jb/mvaf029

Daisuke Tsuji, Nodoka Ishida, Takafumi Miyamoto, Sachiye Inouye, Reiko Akagi

{"title":"Acquisition mechanism of heme oxygenase-1 induction by heat shock in human monocytic cell line THP-1 after differentiation to macrophage-like cells.","authors":"Daisuke Tsuji, Nodoka Ishida, Takafumi Miyamoto, Sachiye Inouye, Reiko Akagi","doi":"10.1093/jb/mvaf029","DOIUrl":"https://doi.org/10.1093/jb/mvaf029","url":null,"abstract":"Heme oxygenase-1 (HO-1) is unique to be directly regulated by diverse stress-responsible transcription factors, however, the cross-talk between oxidative stress and heat shock stress has not been completely elucidated. It is widely accepted that HO activity is not induced by heat shock in cultured cells derived from humans and mice but from rats. Previously, we reported that the discrepancies in heat shock-induced HO-1 expression in different animal species were caused by the access of heat shock factor 1 (HSF1) to heat shock element (HSE) in the different region of the HO-1 gene. Recently, we found that the human monocyte-derived cell line THP-1, which has been extensively used to study monocyte/macrophage functions, represents the heat shock induction of HO-1 after differentiation to macrophage-like cells, although not responsible before differentiation. In this study, we demonstrated that heat shock loading to macrophage-like cells derived from THP-1 specifically activated HSF1 to bind to HSE in the promotor region in the HO-1 gene, resulting in the induction of HO-1. Our finding is significant in understanding the regulation system by macrophages for inflammation caused by oxidative insults and associated with hyperthermia in vivo.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187100","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

Suicide substrate reaction-like modification of mouse serine racemase with L-serine. l -丝氨酸修饰小鼠丝氨酸消旋酶的自杀底物样反应。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-05-30 DOI: 10.1093/jb/mvaf019

Akari Hata, Tomokazu Ito, Hitoshi Mori, Takuya Ogawa, Tatsuo Kurihara, Hisashi Hemmi, Tohru Yoshimura

{"title":"Suicide substrate reaction-like modification of mouse serine racemase with L-serine.","authors":"Akari Hata, Tomokazu Ito, Hitoshi Mori, Takuya Ogawa, Tatsuo Kurihara, Hisashi Hemmi, Tohru Yoshimura","doi":"10.1093/jb/mvaf019","DOIUrl":"10.1093/jb/mvaf019","url":null,"abstract":"A pyridoxal 5'-phosphate-dependent fold-type II serine racemase (SR) is responsible for the synthesis of D-Ser, which serves as a co-agonist of N-methyl-D-aspartate glutamate receptor. In addition to racemization, SR catalyzes the dehydration of D- and L-Ser. SR is suggested to be involved in the D-Ser degradation in vivo, but this has not been confirmed. In this study, we found that mouse SR (mSR) underwent a suicide substrate reaction-like modification with its substrate, resulting in a remarkable change in its reaction specificity. mSR gradually lost its activity by the incubation with L- and D-Ser, but not completely. mSR was labelled with [14C]-L-Ser. ESI-MS analysis revealed that the molecular mass of SR increased by 84 Da by the incubation with L-Ser. Taken together with the results of previous crystallographic studies of fission yeast SR, we concluded that the active site lysine residue of mSR was modified with an α-aminoacrylate intermediate generated from L-Ser and converted to a lysinoalanine residue. The modification significantly decreased the racemization and L-Ser dehydration activities, while dramatically increased the D-Ser dehydration activity by the ~100 times reduction of the Km value. This is probably advantageous for the D-Ser degradation by mSR under physiological conditions.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"437-445"},"PeriodicalIF":2.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998817","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

The potential of erythrocyte α-synuclein to differentiate dementia with Lewy bodies from Parkinson's and Alzheimer's diseases. 红细胞α-突触核蛋白鉴别路易体痴呆与帕金森病和阿尔茨海默病的潜力。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-05-30 DOI: 10.1093/jb/mvaf017

Ryosuke Amagai, Ryunosuke Hosoi, Sakura Yoshioka, Taiki Maruyama, Takayuki Kawai, Soroku Yagihashi, Hitoshi Nukada, Ryuji Sakakibara, Ayako Okado-Matsumoto

{"title":"The potential of erythrocyte α-synuclein to differentiate dementia with Lewy bodies from Parkinson's and Alzheimer's diseases.","authors":"Ryosuke Amagai, Ryunosuke Hosoi, Sakura Yoshioka, Taiki Maruyama, Takayuki Kawai, Soroku Yagihashi, Hitoshi Nukada, Ryuji Sakakibara, Ayako Okado-Matsumoto","doi":"10.1093/jb/mvaf017","DOIUrl":"10.1093/jb/mvaf017","url":null,"abstract":"Dementia with Lewy bodies (DLB) is the second most common neurodegenerative dementia after Alzheimer's disease (AD). Early differentiation of these disorders is crucial for managing core symptoms; however, existing biomarkers remain insufficient. DLB shares motor and cognitive symptoms with Parkinson's disease (PD), and both are classified as synucleinopathies due to abnormal α-synuclein aggregation. Although α-synuclein is predominantly expressed in the central nervous system, it is also abundant in erythrocytes. Recent studies suggest a potential link between erythrocyte-derived α-synuclein and synucleinopathy pathology. Additionally, we previously reported that both erythrocytes and circulating medium and large extracellular vesicles (m/lEVs) in plasma from healthy subjects contain full-length and C-terminally truncated α-synuclein. In this study, we found that erythrocyte α-synuclein levels were significantly lower in DLB compared to AD, PD and healthy controls. Furthermore, α-synuclein levels in circulating m/lEVs were elevated in patients with neurodegenerative diseases. These findings provide new insights into the role of peripheral α-synuclein and suggest its potential utility as a diagnostic marker for DLB. While further validation is needed, erythrocyte-derived α-synuclein may complement nuclear medicine assessments in distinguishing DLB from other neurodegenerative disorders.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"415-424"},"PeriodicalIF":2.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007450","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

YTHDF1 promotes pancreatic cancer cell progression by enhancing SF3B2 translation though m6A modification. YTHDF1通过m6A修饰增强SF3B2翻译促进胰腺癌细胞进展。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-05-30 DOI: 10.1093/jb/mvaf018

Chunyang Wang, Kai Huang, Jie Yang, Qingchun Xu, Jiagao Kuai, Guangxian Zhang, Xiaoming Wang

{"title":"YTHDF1 promotes pancreatic cancer cell progression by enhancing SF3B2 translation though m6A modification.","authors":"Chunyang Wang, Kai Huang, Jie Yang, Qingchun Xu, Jiagao Kuai, Guangxian Zhang, Xiaoming Wang","doi":"10.1093/jb/mvaf018","DOIUrl":"10.1093/jb/mvaf018","url":null,"abstract":"N6-Methyladenosine (m6A), a pivotal RNA modification, plays a critical role in carcinogenesis across multiple cancer types. YT521-B homology domain family protein 1 (YTHDF1), a binding protein of m6A, facilitates the translation of downstream targets via m6A recognition. However, the involvement of YTHDF1 in pancreatic cancer progression and its mechanistic underpinnings remain poorly understood. In this study, we observed significant upregulation of YTHDF1 in pancreatic cancer cell lines (SW1990 and PANC-1) compared to the normal human pancreatic cell line hTERT-HPNE. Functional assays revealed that YTHDF1 knockdown markedly suppressed cell proliferation and invasion, whereas its overexpression enhanced these malignant phenotypes in both SW1990 and PANC-1 cells. Mechanistically, YTHDF1 interacted with coding sequence (CDS) region of splicing factor 3B subunit 2 (SF3B2), whereas YTHDF1 downregulation reduced SF3B2 protein levels without altering its mRNA expression, suggesting post-transcriptional regulation via m6A modification. Importantly, SF3B2 overexpression rescued the suppressed proliferation and invasion caused by YTHDF1 knockdown in SW1990 and PANC-1 cells. Collectively, our findings demonstrate that YTHDF1 drives pancreatic cancer progression by enhancing SF3B2 translation through m6A modification, thereby providing novel mechanistic insights and a potential therapeutic target for pancreatic cancer.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"425-435"},"PeriodicalIF":2.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002305","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

Suppression of ATP-dependent (S)-NAD(P)H-hydrate dehydratase expression inhibits adipocyte differentiation of 3T3-L1 preadipocytes by increasing excessive accumulation of NADHX. 抑制atp依赖性(S)-NAD(P)H-hydrate dehydratase表达通过增加NADHX的过度积累抑制3T3-L1前脂肪细胞的脂肪细胞分化。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-05-30 DOI: 10.1093/jb/mvaf015

Kazuki Nakajima, Kodai Takahashi, Masako Tanaka, Mina Kawashima, Koshi Machida, Yoichi Nakao, Keiyo Takubo, Nobuhito Goda

{"title":"Suppression of ATP-dependent (S)-NAD(P)H-hydrate dehydratase expression inhibits adipocyte differentiation of 3T3-L1 preadipocytes by increasing excessive accumulation of NADHX.","authors":"Kazuki Nakajima, Kodai Takahashi, Masako Tanaka, Mina Kawashima, Koshi Machida, Yoichi Nakao, Keiyo Takubo, Nobuhito Goda","doi":"10.1093/jb/mvaf015","DOIUrl":"10.1093/jb/mvaf015","url":null,"abstract":"ATP-dependent (S)-NAD(P)H-hydrate dehydratase (NAXD) is a crucial enzyme in the nicotinamide adenine dinucleotide repair system that regenerates NAD(P)H, an essential electron donor in metabolic redox reactions. NAD+-related metabolic pathways connect cellular metabolism and the expression of genes responsible for adipogenesis; however, the biological significance of the NAXD-mediated repair pathway remains unclear. Herein, we showed that NAXD is essential for normal adipocyte differentiation of 3T3-L1 murine preadipocytes. Silencing of the Naxd gene attenuated differentiation-induced lipid accumulation with excessive accumulation of hydrated NADH (NADHX) without altering NAD+ levels. FK866, a specific inhibitor of NAMPT, further reduced lipid accumulation even in Naxd-silenced cells with substantial decrease in NAD+. Supplementation with nicotinamide mononucleotide, a precursor of NAD+, restored NAD+ levels comparably in Naxd- and LacZ-silenced cells treated with FK866, but failed to recover adipocyte differentiation of Naxd-silenced cells to the level of LacZ-silenced cells. In contrast, exposure of wild-type 3T3-L1 cells to NADHX recapitulated the Naxd deficiency-elicited inhibitory effects on adipocyte differentiation with reduced expression of master transcriptional regulators of adipogenesis, peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α. These results suggest that NAXD supports normal adipogenesis, in part, by inhibiting excessive accumulation of NADHX.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"403-414"},"PeriodicalIF":2.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12136578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of N1-methyladenosine in the quantification of RNA. n1 -甲基腺苷在RNA定量中的作用。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-05-30 DOI: 10.1093/jb/mvaf014

Fangran Liu

引用次数: 0