Biochimica et biophysica acta. General subjects最新文献

{"title":"The K346T mutant of GnT-III bearing weak in vitro and potent intracellular activity","authors":"Yuta Hashimoto ,&nbsp;Haruka Kawade ,&nbsp;WanXue Bao ,&nbsp;Sayaka Morii ,&nbsp;Miyako Nakano ,&nbsp;Masamichi Nagae ,&nbsp;Reiko Murakami ,&nbsp;Yuko Tokoro ,&nbsp;Misaki Nakashima ,&nbsp;Zixuan Cai ,&nbsp;Tomoya Isaji ,&nbsp;Jianguo Gu ,&nbsp;Kazuki Nakajima ,&nbsp;Yasuhiko Kizuka","doi":"10.1016/j.bbagen.2024.130663","DOIUrl":"10.1016/j.bbagen.2024.130663","url":null,"abstract":"<div><h3>Background</h3><p><em>N</em>-Acetylglucosaminyltransferase-III (GnT-III, also designated MGAT3) catalyzes the formation of a specific <em>N</em>-glycan branch, bisecting GlcNAc, in the Golgi apparatus. Bisecting GlcNAc is a key residue that suppresses <em>N</em>-glycan maturation and is associated with the pathogenesis of cancer and Alzheimer's disease. However, it remains unclear how GnT-III recognizes its substrates and how GnT-III activity is regulated in cells.</p></div><div><h3>Methods</h3><p>Using AlphaFold2 and structural comparisons, we predicted the key amino acid residues in GnT-III that interact with substrates in the catalytic pocket. We also performed <em>in vitro</em> activity assay, lectin blotting analysis and <em>N</em>-glycomic analysis using point mutants to assess their activity.</p></div><div><h3>Results</h3><p>Our data suggested that E320 of human GnT-III is the catalytic center. More interestingly, we found a unique mutant, K346T, that exhibited lower <em>in vitro</em> activity and higher intracellular activity than wild-type GnT-III. The enzyme assays using various substrates showed that the substrate specificity of K346T was unchanged, whereas cycloheximide chase experiments revealed that the K346T mutant has a slightly shorter half-life, suggesting that the mutant is unstable possibly due to a partial misfolding. Furthermore, TurboID-based proximity labeling showed that the localization of the K346T mutant is shifted slightly to the <em>cis</em> side of the Golgi, probably allowing for prior action to competing galactosyltransferases.</p></div><div><h3>Conclusions</h3><p>The slight difference in K346T localization may be responsible for the higher biosynthetic activity despite the reduced activity.</p></div><div><h3>General significance</h3><p>Our findings underscore the importance of fine intra-Golgi localization and reaction orders of glycosyltransferases for the biosynthesis of complex glycan structures in cells.</p></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 9","pages":"Article 130663"},"PeriodicalIF":2.8,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141465914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncolytic virotherapy improves immunotherapies targeting cancer stemness in glioblastoma","authors":"Mohsen Keshavarz ,&nbsp;Hassan Dianat-Moghadam ,&nbsp;Seyedeh Sara Ghorbanhosseini ,&nbsp;Behrang Sarshari","doi":"10.1016/j.bbagen.2024.130662","DOIUrl":"10.1016/j.bbagen.2024.130662","url":null,"abstract":"<div><p>Despite advances in cancer therapies, glioblastoma (GBM) remains the most resistant and recurrent tumor in the central nervous system. GBM tumor microenvironment (TME) is a highly dynamic landscape consistent with alteration in tumor infiltration cells, playing a critical role in tumor progression and invasion. In addition, glioma stem cells (GSCs) with self-renewal capability promote tumor recurrence and induce therapy resistance, which all have complicated eradication of GBM with existing therapies. Oncolytic virotherapy is a promising field of therapy that can kill tumor cells in a targeted manner. Manipulated oncolytic viruses (OVs) improve cancer immunotherapy by directly lysis tumor cells, infiltrating antitumor cells, inducing immunogenic cell death, and sensitizing immune-resistant TME to an immune-responsive hot state. Importantly, OVs can target stemness–driven GBM progression. In this review, we will discuss how OVs as a therapeutic option target GBM, especially the GSC subpopulation, and induce immunogenicity to remodel the TME, which subsequently enhances immunotherapies' efficiency.</p></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 9","pages":"Article 130662"},"PeriodicalIF":2.8,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic regulation of abiotic stress responses in plants","authors":"Shilpa ,&nbsp;Rajnikant Thakur ,&nbsp;Pramod Prasad","doi":"10.1016/j.bbagen.2024.130661","DOIUrl":"10.1016/j.bbagen.2024.130661","url":null,"abstract":"<div><p>Plants face a wide array of challenges in their environment, both from living organisms (biotic stresses) and non-living factors (abiotic stresses). Among the major abiotic stressors affecting crop plants, variations in temperature, water availability, salinity, and cold pose significant threats to crop yield and the quality of produce. Plants possess remarkable adaptability and resilience, and they employ a range of genetic and epigenetic mechanisms to respond and cope with abiotic stresses. A few crucial set of epigenetic mechanisms that support plants in their battle against these stresses includes DNA methylation and histone modifications. These mechanisms play a pivotal role in enabling plants to endure and thrive under challenging environmental conditions. The mechanisms of different epigenetic mechanisms in responding to the abiotic stresses vary. Each plant species and type of stress may trigger distinct epigenetic responses, highlighting the complexity of the plant's ability to adapt under stress conditions. This review focuses on the paramount importance of epigenetics in enhancing a plant's ability to survive and excel under various abiotic stresses. It highlights recent advancements in our understanding of the epigenetic mechanisms that contribute to abiotic stress tolerance in plants. This growing knowledge is pivotal for shaping future efforts aimed at mitigating the impact of abiotic stresses on diverse crop plants.</p></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 9","pages":"Article 130661"},"PeriodicalIF":3.0,"publicationDate":"2024-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141401891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Caveolin-1 differentially regulates the transforming growth factor-β and epidermal growth factor signaling pathways in MDCK cells","authors":"Shih-Chuan Hsiao ,&nbsp;Wei-Hsiang Liao ,&nbsp;Heng-Ai Chang ,&nbsp;Yi-Shyun Lai ,&nbsp;Ta-Wei Chan ,&nbsp;Ying-Chi Chen ,&nbsp;Wen-Tai Chiu","doi":"10.1016/j.bbagen.2024.130660","DOIUrl":"10.1016/j.bbagen.2024.130660","url":null,"abstract":"<div><p>Caveolin-1 is critical for interacting with the TGF-β receptor (TGFβR) and EGF receptor (EGFR) signaling, often observed in advanced cancers and tissue fibrosis. However, the mechanism underlying caveolin-1-mediated transactivation of TGFβR and EGFR signaling remains unclear. Therefore, we sought to determine whether caveolin-1 is involved in canonical and non-canonical TGFβR and EGFR signaling transactivation in this study. Methyl-β-cyclodextrin (MβCD) was used to disrupt the cholesterol-containing membranes domains, and the caveolin-1 scaffolding domain (CSD) peptide was used to mimic the CSD of caveolin-1. Additionally, we transfected the Madin-Darby canine kidney cells with wild-type or phosphorylation-defective caveolin-1. We discovered that tyrosine 14 of caveolin-1 was critical for the negative regulation of TGFβR and EGFR canonical signaling. On the contrary, caveolin-1 inhibited TGF-β1-induced ERK2 activation independent of tyrosine 14 phosphorylation. Although EGF failed to induce Smad3 phosphorylation in caveolin-1 knockdown cells, it activated Smad3 upon MβCD co-treatment, indicating that caveolin-1 indirectly regulated the non-canonical pathway of EGF. In conclusion, caveolin-1 differentially modulates TGFβR and EGFR signaling. Thus, targeting caveolin-1 is a potential strategy for treating diseases involving TGF-β1 and EGF signaling.</p></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 9","pages":"Article 130660"},"PeriodicalIF":3.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S030441652400103X/pdfft?md5=7ca4b4262ec73d5cd7af72b2c7eee186&pid=1-s2.0-S030441652400103X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141316608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Products of oxidative and non-oxidative metabolism of L-arginine as potential regulators of Ca2+ transport in mitochondria of uterine smooth muscle","authors":"Hanna V. Danylovych,&nbsp;Yuriy V. Danylovych,&nbsp;Maksym R. Pavliuk,&nbsp;Sergiy O. Kosterin","doi":"10.1016/j.bbagen.2024.130652","DOIUrl":"10.1016/j.bbagen.2024.130652","url":null,"abstract":"<div><p>Mitochondria play a crucial role in maintaining Ca²⁺ homeostasis in cells. Due to the critical regulatory role of the products of oxidative and non-oxidative metabolism of L-arginine, it is essential to clarify their effect on Ca²⁺ transport in smooth muscle mitochondria.</p><p>Experiments were performed on the uterine myocytes of rats and isolated mitochondria. The possibility of NO synthesis by mitochondria was demonstrated by confocal microscopy and spectrofluorimetry methods using the NO-sensitive fluorescent probe DAF-FM and Mitotracker Orange CM-H2TMRos. It was shown that 50 μM L-arginine stimulates the energy-dependent accumulation of Ca²⁺ in mitochondria using the fluorescent probe Fluo-4 AM. A similar effect occurred when using nitric oxide donors 100 μM SNP, SNAP, and sodium nitrite (SN) directly. The stimulating effect was eliminated in the presence of the NO scavenger C-PTIO. Nitric oxide reduces the electrical potential in mitochondria without causing them to swell. The stimulatory effect of spermine on the accumulation of Ca²⁺ by mitochondria is attributed to the enhancement of NO synthesis, which was demonstrated with the use of C-PTIO, NO-synthase inhibitors (100 μM NA and L-NAME), as well as by direct monitoring of NO synthesis fluorescent probe DAF-FM.</p><p>A conclusion was drawn about the potential regulatory effect of the product of the oxidative metabolism of L-arginine – NO on the transport of Ca²⁺ in the mitochondria of the myometrium, as well as the corresponding effect of the product of non-oxidative metabolism –spermine by increasing the synthesis of NO in these subcellular structures.</p></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 9","pages":"Article 130652"},"PeriodicalIF":3.0,"publicationDate":"2024-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141299908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of RAGE in radiation-induced acquisition of malignant phenotypes in human glioblastoma cells","authors":"Hiromu Seki ,&nbsp;Kazuki Kitabatake ,&nbsp;Sei-ichi Tanuma ,&nbsp;Mitsutoshi Tsukimoto","doi":"10.1016/j.bbagen.2024.130650","DOIUrl":"10.1016/j.bbagen.2024.130650","url":null,"abstract":"<div><p>Glioblastoma (GBM), a highly aggressive malignant tumor of the central nervous system, is mainly treated with radiotherapy. However, since irradiation may lead to the acquisition of migration ability by cancer cells, thereby promoting tumor metastasis and invasion, it is important to understand the mechanism of cell migration enhancement in order to prevent recurrence of GBM. The receptor for advanced glycation end products (RAGE) is a pattern recognition receptor activated by high mobility group box 1 (HMGB1). In this study, we found that RAGE plays a role in the enhancement of cell migration by γ-irradiation in human GBM A172 cells. γ-Irradiation induced actin remodeling, a marker of motility acquisition, and enhancement of cell migration in A172 cells. Both phenotypes were suppressed by specific inhibitors of RAGE (FPS-ZM1 and TTP488) or by knockdown of RAGE. The HMGB1 inhibitor ethyl pyruvate similarly suppressed γ-irradiation-induced enhancement of cell migration. In addition, γ-irradiation-induced phosphorylation of STAT3 was suppressed by RAGE inhibitors, and a STAT3 inhibitor suppressed γ-irradiation-induced enhancement of cell migration, indicating that STAT3 is involved in the migration enhancement downstream of RAGE. Our results suggest that HMGB1-RAGE-STAT3 signaling is involved in radiation-induced enhancement of GBM cell migration, and may contribute to GBM recurrence by promoting metastasis and invasion.</p></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 9","pages":"Article 130650"},"PeriodicalIF":3.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S030441652400093X/pdfft?md5=5d472348e632dffff6f54213768fc75c&pid=1-s2.0-S030441652400093X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141236954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential involvement of KANK1 haploinsufficiency in centrosome aberrations","authors":"Ikumi Imamura,&nbsp;Ryoiti Kiyama","doi":"10.1016/j.bbagen.2024.130648","DOIUrl":"10.1016/j.bbagen.2024.130648","url":null,"abstract":"<div><p><em>KANK1</em> was found as a tumor suppressor gene based on frequent deletions in renal cell carcinoma and the inhibitory activity of tumor cell proliferation. Previously, we reported that knockdown of <em>KANK1</em> induced centrosomal amplification, leading to abnormal cell division, through the hyperactivation of RhoA small GTPase. Here, we investigated the loss of <em>KANK1</em> function by performing CRISPR/Cas9-based genome editing to knockout the gene. After several rounds of genome editing, however, there were no cell lines with complete loss of <em>KANK1</em>, and the less the wild-type <em>KANK1</em> dosage, the greater the number of cells with abnormal numbers of centrosomes and rates of cell-doubling and apoptosis, suggesting the involvement of <em>KANK1</em> haploinsufficiency in centrosome aberrations. The rescue of <em>KANK1</em>-knockdown cells with a <em>KANK1</em>-expressing plasmid restored the rates of cells exhibiting centrosomal amplification to the control level. RNA-sequencing analysis of the cells with reduced dosages of functional <em>KANK1</em> revealed potential involvement of other cell proliferation-related genes, such as <em>EGR1</em>, <em>MDGA2</em>, and <em>BMP3</em>, which have been reported to show haploinsufficiency when they function. When EGR1 protein expression was reduced by siRNA technology, the number of cells exhibiting centrosomal amplification increased, along with the reduction of KANK1 protein expression, suggesting their functional relationship. Thus, <em>KANK1</em> haploinsufficiency may contribute to centrosome aberrations through the network of haploinsufficiency-related genes.</p></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 8","pages":"Article 130648"},"PeriodicalIF":3.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141236961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cannabidiol reverts the malignant phenotype of hepatocellular carcinoma cells via the GPR55/TP53/MAPK axis","authors":"Shirui Tan ,&nbsp;Qamar uz Zaman ,&nbsp;Shah Fahad ,&nbsp;Gang Deng","doi":"10.1016/j.bbagen.2024.130651","DOIUrl":"10.1016/j.bbagen.2024.130651","url":null,"abstract":"<div><p>Cannabidiol (CBD) has antioxidant and anti-inflammatory activities. However, the anti-tumor effect of CBD on hepatocellular carcinoma (HCC) remains unclear. Here, we investigated whether CBD displays anti-tumorigenic effects in HCC cells and whether it could reduce tumorigenesis and metastases <em>in vivo</em>. First, this study treated HCC cells with different concentrations of CBD, followed by analyzing the changes in the proliferative, apoptotic, migratory and invasive abilities. The effects of CBD on the growth and metastasis of HCC cells <em>in vivo</em> were verified by tumorigenesis and metastasis assays. Subsequently, the target genes of CBD were predicted through the SwissTarget website and the genes differentially expressed in cells after CBD treatment were analyzed by microarray for intersection. The enrichment of the pathways after CBD treatment was analyzed by KEGG enrichment analysis, followed by western blot validation. Finally, rescue assays were used to validate the functions of genes as well as pathways in the growth and metastasis of HCC cells. A significant weakening of the ability of HCC cells to grow and metastasize <em>in vitro</em> and <em>in vivo</em> was observed upon CBD treatment. Mechanistically, CBD reduced GRP55 expression in HCC cells, along with increased TP53 expression and blocked MAPK signaling activation. In CBD-treated cells, the anti-tumor of HCC cells was restored after overexpression of GRP55 or deletion of TP53. CBD inhibits the MAPK signaling activation and increases the TP53 expression by downregulating GRP55 in HCC cells, thereby suppressing the growth and metastasis of HCC cells.</p></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 8","pages":"Article 130651"},"PeriodicalIF":3.0,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141198779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca2+ mobilization irrespectively of its primary target","authors":"Polina D. Kotova,&nbsp;Ekaterina A. Dymova,&nbsp;Oleg O. Lyamin,&nbsp;Olga A. Rogachevskaja,&nbsp;Stanislav S. Kolesnikov","doi":"10.1016/j.bbagen.2024.130649","DOIUrl":"10.1016/j.bbagen.2024.130649","url":null,"abstract":"<div><p>The phosphoinositide 3-kinase (PI3K) is involved in regulation of multiple intracellular processes. Although the inhibitory analysis is generally employed for validating a physiological role of PI3K, increasing body of evidence suggests that PI3K inhibitors can exhibit PI3K-unrelated activity as well. Here we studied Ca²⁺ signaling initiated by aminergic agonists in a variety of different cells and analyzed effects of the PI3K inhibitor PI828 on cell responsiveness. It turned out that PI828 inhibited Ca²⁺ transients elicited by acetylcholine (ACh), histamine, and serotonin, but did not affect Ca²⁺ responses to norepinephrine and ATP. Another PI3K inhibitor wortmannin negligibly affected Ca²⁺ signaling initiated by any one of the tested agonists. Using the genetically encoded PIP₃ sensor PH(Akt)-Venus, we confirmed that both PI828 and wortmannin effectively inhibited PI3K and ascertained that this kinase negligibly contributed to ACh transduction. These findings suggested that PI828 inhibited Ca²⁺ responses to aminergic agonists tested, involving an unknown cellular mechanism unrelated to the PI3K inhibition. Complementary physiological experiments provided evidence that PI828 could inhibit Ca²⁺ signals induced by certain agonists, by acting extracellularly, presumably, through their surface receptors. For the muscarinic M3 receptor, this possibility was verified with molecular docking and molecular dynamics. As demonstrated with these tools, wortmannin could be bound in the extracellular vestibule at the muscarinic M3 receptor but this did not preclude binding of ACh to the M3 receptor followed by its activation. In contrast, PI828 could sterically block the passage of ACh into the allosteric site, preventing activation of the muscarinic M3 receptor.</p></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 8","pages":"Article 130649"},"PeriodicalIF":3.0,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “CAMSAP3-mediated regulation of HMGB1 acetylation and subcellular localization in lung cancer cells: Implications for cell death modulation”. [BBA - General Subjects (2024) 1868: 130614]","authors":"N. Singharajkomron ,&nbsp;S. Seephan ,&nbsp;I. Iksen ,&nbsp;N. Chantaravisoot ,&nbsp;P. Wongkongkathep ,&nbsp;Y. Hayakawa ,&nbsp;V. Pongrakhananon","doi":"10.1016/j.bbagen.2024.130644","DOIUrl":"10.1016/j.bbagen.2024.130644","url":null,"abstract":"","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1868 8","pages":"Article 130644"},"PeriodicalIF":3.0,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0304416524000874/pdfft?md5=13220e11ad02488330338df5b91c7222&pid=1-s2.0-S0304416524000874-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141173947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}