Cell Cycle最新文献

{"title":"Inhibition of endogenous hydrogen sulfide production reduces activation of hepatic stellate cells via the induction of cellular senescence.","authors":"Turtushikh Damba, Mengfan Zhang, Sandra A Serna Salas, Zongmei Wu, Harry van Goor, Aaron Fierro Arenas, Martin Humberto Muñoz-Ortega, Javier Ventura-Juárez, Manon Buist-Homan, Han Moshage","doi":"10.1080/15384101.2024.2345477","DOIUrl":"10.1080/15384101.2024.2345477","url":null,"abstract":"<p><p>In chronic liver injury, quiescent hepatic stellate cells (HSCs) transdifferentiate into activated myofibroblast-like cells and produce large amounts of extracellular matrix components, e.g. collagen type 1. Cellular senescence is characterized by irreversible cell-cycle arrest, arrested cell proliferation and the acquisition of the senescence-associated secretory phenotype (SASP) and reversal of HSCs activation. Previous studies reported that H₂S prevents induction of senescence via its antioxidant activity. We hypothesized that inhibition of endogenous H₂S production induces cellular senescence and reduces activation of HSCs. Rat HSCs were isolated and culture-activated for 7 days. After activation, HSCs treated with H₂S slow-releasing donor GYY4137 and/or DL-propargylglycine (DL-PAG), an inhibitor of the H2S-producing enzyme cystathionine γ-lyase (CTH), as well as the PI3K inhibitor LY294002. In our result, CTH expression was significantly increased in fully activated HSCs compared to quiescent HSCs and was also observed in activated stellate cells in a <i>in vivo</i> model of cirrhosis. Inhibition of CTH reduced proliferation and expression of fibrotic markers <i>Col1a1</i> and <i>Acta2</i> in HSCs. Concomitantly, DL-PAG increased the cell-cycle arrest markers <i>Cdkn1a (p21)</i>, <i>p53</i> and the SASP marker <i>Il6</i>. Additionally, the number of β-galactosidase positive senescent HSCs was increased. GYY4137 partially restored the proliferation of senescent HSCs and attenuated the DL-PAG-induced senescent phenotype. Inhibition of PI3K partially reversed the senescence phenotype of HSCs induced by DL-PAG. Inhibition of endogenous H₂S production reduces HSCs activation via induction of cellular senescence in a PI3K-Akt dependent manner. Our results show that cell-specific inhibition of H₂S could be a novel target for anti-fibrotic therapy via induced cell senescence.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11229775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141246748","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":"Therapy-induced senescence is finally escapable, what is next?","authors":"Tareq Saleh","doi":"10.1080/15384101.2024.2364579","DOIUrl":"10.1080/15384101.2024.2364579","url":null,"abstract":"<p><p>Several breakthrough articles have recently confirmed the ability of tumor cells to escape the stable cell cycle arrest imposed by Therapy-Induced Senescence (TIS). Subsequently, accepting the hypothesis that TIS is escapable should encourage serious reassessments of the fundamental roles of senescence in cancer treatment. The potential for escape from TIS undermines the well-established tumor suppressor function of senescence, proposes it as a mechanism of tumor dormancy leading to disease recurrence and invites for further investigation of its unfavorable contribution to cancer therapy outcomes. Moreover, escaping TIS strongly indicates that the elimination of senescent tumor cells, primarily through pharmacological means, is a suitable approach for increasing the efficacy of cancer treatment, one that still requires further exploration. This commentary provides an overview of the recent evidence that unequivocally demonstrated the ability of therapy-induced senescent tumor cells in overcoming the terminal growth arrest fate and provides future perspectives on the roles of TIS in tumor biology.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11229739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141327281","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":"Sustained activation of NF-κB through constitutively active IKKβ leads to senescence bypass in murine dermal fibroblasts.","authors":"Masayuki Harada, Kanae Su-Harada, Takeshi Kimura, Koh Ono, Noboru Ashida","doi":"10.1080/15384101.2024.2325802","DOIUrl":"10.1080/15384101.2024.2325802","url":null,"abstract":"<p><p>Although the transcription factor nuclear factor κB (NF-κB) plays a central role in the regulation of senescence-associated secretory phenotype (SASP) acquisition, our understanding of the involvement of NF-κB in the induction of cellular senescence is limited. Here, we show that activation of the canonical NF-κB pathway suppresses senescence in murine dermal fibroblasts. IκB kinase β (IKKβ)-depleted dermal fibroblasts showed ineffective NF-κB activation and underwent senescence more rapidly than control cells when cultured under 20% oxygen conditions, as indicated by senescence-associated β-galactosidase (SA-β-gal) staining and <i>p16^INK4a</i> mRNA levels. Conversely, the expression of <u>c</u>onstitutively <u>a</u>ctive IKKβ (IKKβ-CA) was sufficient to drive senescence bypass. Notably, the expression of a degradation-resistant form of inhibitor of κB (IκB), which inhibits NF-κB nuclear translocation, abolished senescence bypass, suggesting that the inhibitory effect of IKKβ-CA on senescence is largely mediated by NF-κB. We also found that IKKβ-CA expression suppressed the derepression of <i>INK4/Arf</i> genes and counteracted the senescence-associated loss of <i>Ezh2</i>, a catalytic subunit of the Polycomb repressive complex 2 (PRC2). Moreover, pharmacological inhibition of Ezh2 abolished IKKβ-CA-induced senescence bypass. We propose that NF-κB plays a suppressive role in the induction of stress-induced senescence through sustaining <i>Ezh2</i> expression.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140093410","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":"Knockdown of hCINAP sensitizes colorectal cancer cells to ionizing radiation.","authors":"Meizhu Shen, Yong Zhang, Fang Wu, Meizhen Shen, Sen Zhang, Yun Guo, Jialiang Gan, Rensheng Wang","doi":"10.1080/15384101.2024.2309015","DOIUrl":"10.1080/15384101.2024.2309015","url":null,"abstract":"<p><p>Colorectal cancer (CRC) poses a significant challenge in terms of treatment due to the prevalence of radiotherapy resistance. However, the underlying mechanisms responsible for radio-resistance in CRC have not been thoroughly explored. This study aimed to shed light on the role of human coilin interacting nuclear ATPase protein (hCINAP) in radiation-resistant HT-29 and SW480 CRC cells (HT-29-IR and SW480-IR) and investigate its potential implications. Firstly, radiation-resistant CRC cell lines were established by subjecting HT-29 and SW480 cells to sequential radiation exposure. Subsequent analysis revealed a notable increase in hCINAP expression in radiation-resistant CRC cells. To elucidate the functional role of hCINAP in radio-resistance, knockdown experiments were conducted. Remarkably, knockdown of hCINAP resulted in an elevation of reactive oxygen species (ROS) generation upon radiation treatment and subsequent activation of apoptosis mediated by mitochondria. These observations indicate that hCINAP depletion enhances the radiosensitivity of CRC cells. Conversely, when hCINAP was overexpressed, it was found to enhance the radio-resistance of CRC cells. This suggests that elevated hCINAP expression contributes to the development of radio-resistance. Further investigation revealed an interaction between hCINAP and ATPase family AAA domain containing 3A (ATAD3A). Importantly, ATAD3A was identified as an essential factor in hCINAP-mediated radio-resistance. These findings establish the involvement of hCINAP and its interaction with ATAD3A in the regulation of radio-resistance in CRC cells. Overall, the results of this study demonstrate that upregulating hCINAP expression may improve the survival of radiation-exposed CRC cells. Understanding the intricate molecular mechanisms underlying hCINAP function holds promise for potential strategies in targeted radiation therapy for CRC. These findings emphasize the importance of further research to gain a comprehensive understanding of hCINAP's precise molecular mechanisms and explore its potential as a therapeutic target in overcoming radio-resistance in CRC. By unraveling the complexities of hCINAP and its interactions, novel therapeutic approaches may be developed to enhance the efficacy of radiation therapy and improve outcomes for CRC patients.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140317856","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":"Expression profile of mRNAs and miRNAs related to mitogen-activated kinases in HaCaT cell culture treated with lipopolysaccharide a and adalimumab.","authors":"Michał Wójcik, Aleksandra Plata-Babula, Amelia Głowaczewska, Tomasz Sirek, Aneta Orczyk, Mariola Małecka, Beniamin Oskar Grabarek","doi":"10.1080/15384101.2024.2335051","DOIUrl":"10.1080/15384101.2024.2335051","url":null,"abstract":"<p><p>Studies indicate that mitogen-activated protein kinases (MAPKs) exhibit activation and overexpression within psoriatic lesions. This study aimed to investigate alterations in the expression patterns of genes encoding MAPKs and microRNA (miRNA) molecules that potentially regulate their expression in human adult low-calcium high-temperature (HaCaT) keratinocytes when exposed to bacterial lipopolysaccharide A (LPS) and adalimumab. HaCaT cells underwent treatment with 1 µg/mL LPS for 8 hours, followed by treatment with 8 µg/mL adalimumab for 2, 8, or 24 hours. Untreated cells served as controls. The molecular analysis involved microarray, quantitative real-time polymerase chain reaction (RTqPCR), and enzyme-linked immunosorbent assay (ELISA) analyses. Changes in the expression profile of seven mRNAs: dual specificity phosphatase 1 (<i>DUSP1)</i>, dual specificity phosphatase 3 (<i>DUSP3)</i>, dual specificity phosphatase 4 (<i>DUSP4)</i>, mitogen-activated protein kinase 9 (<i>MAPK9)</i>, mitogen-activated protein kinase kinase kinase 2 (<i>MAP3K2)</i>, mitogen-activated protein kinase kinase 2 (<i>MAP2K2), and</i> MAP kinase-activated protein kinase 2 <i>(MAPKAPK2</i>, also known as <i>MK2)</i> in cell culture exposed to LPS or LPS and the drug compared to the control. It was noted that miR-34a may potentially regulate the activity of <i>DUSP1</i>, <i>DUSP3</i>, and <i>DUSP4</i>, while miR-1275 is implicated in regulating <i>MAPK9</i> expression. Additionally, miR-382 and miR-3188 are potential regulators of <i>DUSP4</i> levels, and miR-200-5p is involved in regulating <i>MAPKAPK2</i> and <i>MAP3K2</i> levels. Thus, the analysis showed that these mRNA molecules and the proteins and miRNAs they encode appear to be useful molecular markers for monitoring the efficacy of adalimumab therapy.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11174132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334830","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":"Extracellular vesicles from <i>Fusobacterium nucleatum</i>: roles in the malignant phenotypes of gastric cancer.","authors":"Xiangkun Meng, Gang Ma, Xu Zhang, Hua Yin, Yu Miao, Fang He","doi":"10.1080/15384101.2024.2324587","DOIUrl":"10.1080/15384101.2024.2324587","url":null,"abstract":"<p><p>The increase of the <i>Fusobacterium nucleatum</i> level has been previously identified in various cancers including gastric cancer (GC), but how the <i>F. nucleatum</i> exerts its carcinogenic role in GC remains unclear. Several studies revealed that <i>F. nucleatum</i> contributes to cancer progression via its secretion of extracellular vehicles (EVs). Hence, it's designed to reveal the influence of <i>F. nucleatum</i>-derived EVs (Fn-EVs) in GC progression. The tumor and adjacent tissues were collected from 30 GC patients, and the abundance of <i>F. nucleatum</i> was found to be highly expressed in tumor samples. The ultracentrifugation was employed to isolate EVs from <i>F. nucleatum</i> and <i>Escherischia coli</i> (<i>E. coli</i>), which were labeled Fn-EVs and <i>E. coli</i>-EVs, respectively. After treating GC cells with Fn-EVs and <i>E. coli</i>-EVs, cell counting kit 8, colony formation, wound healing as well as transwell assay were performed, which revealed that Fn-EVs effectively enhanced oxaliplatin resistance, and facilitated cell proliferation, migration, invasion, and stemness in GC cells while <i>E. coli</i>-EVs exert no significant effect on GC cells. Besides, the stemness and DNA repair of GC cells were also enhanced by Fn-EVs, as revealed by the sphere-forming assay and the detection of stemness- and DNA repair-associated proteins by western blotting. <i>In vivo</i> analyses demonstrated that Fn-EVs administration not only promoted GC tumor growth and liver metastasis but also conferred GC tumor resistance to oxaliplatin resistance. This study first revealed the contributive role of <i>F. nucleatum</i> in GC development via Fn-EVs, which provided a better perspective for manipulating <i>F. nucleatum</i> in treating GC patients with malignant phenotypes.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140038750","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":"REV7-p53 interaction inhibits ATM-mediated DNA damage signaling.","authors":"Megan Biller, Sara Kabir, Chkylle Boado, Sarah Nipper, Alexandra Saffa, Ariella Tal, Sydney Allen, Hiroyuki Sasanuma, Didier Dréau, Cyrus Vaziri, Junya Tomida","doi":"10.1080/15384101.2024.2333227","DOIUrl":"10.1080/15384101.2024.2333227","url":null,"abstract":"<p><p>REV7 is an abundant, multifunctional protein that is a known factor in cell cycle regulation and in several key DNA repair pathways including Trans-Lesion Synthesis (TLS), the Fanconi Anemia (FA) pathway, and DNA Double-Strand Break (DSB) repair pathway choice. Thus far, no direct role has been studied for REV7 in the DNA damage response (DDR) signaling pathway. Here we describe a novel function for REV7 in DSB-induced p53 signaling. We show that REV7 binds directly to p53 to block ATM-dependent p53 Ser15 phosphorylation. We also report that REV7 is involved in the destabilization of p53. These findings affirm REV7's participation in fundamental cell cycle and DNA repair pathways. Furthermore, they highlight REV7 as a critical factor for the integration of multiple processes that determine viability and genome stability.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11174130/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334831","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":"Hyaluronidase inhibitor sHA2.75 alleviates ischemia-reperfusion-induced acute kidney injury.","authors":"Yang Zhang, Huajiang Zhao, Jing Zhang","doi":"10.1080/15384101.2024.2309019","DOIUrl":"10.1080/15384101.2024.2309019","url":null,"abstract":"<p><p>Hyaluronidases (HAases) are enzymes that degrade hyaluronic acid (HA) in the animal kingdom. The HAases-HA system is crucial for HA homeostasis and plays a significant role in biological processes and extracellular matrix (ECM)-related pathophysiological conditions. This study aims to explore the role of inhibiting the HAases-HA system in acute kidney injury (AKI). We selected the potent inhibitor \"sHA2.75\" to inhibit HAase activity through mixed inhibitory mechanisms. The ischemia-reperfusion mouse model was established using male BALB/c mice (7-9 weeks old), and animals were subjected to subcapsular injection with 50 mg/kg sHA2.75 twice a week to evaluate the effects of sHA2.75 on AKI on day 1, 5 and 14 after ischemia-reperfusion or sham procedure. Blood and tissue samples were collected for immunohistochemistry, biochemical, and quantitative analyses. sHA2.75 significantly reduced blood urea nitrogen (BUN) and serum creatinine levels in AKI mouse models. Expression of kidney injury-related genes such as Kidney injury molecule-1 (KIM-1), Neutrophil Gelatinase-Associated Lipocalin (NGAL), endothelial nitric oxide synthase (eNOS), type I collagen (Col1), type III collagen (Col3), alpha-smooth muscle actin (α-SMA) showed significant downregulation in mouse kidney tissues after sHA2.75 treatment. Moreover, sHA2.75 treatment led to decreased plasma levels of Interleukin-6 (IL-6) proteins and reduced mRNA levels in renal tissues of AKI mice. Inhibitor sHA2.75 administration in the AKI mouse model downregulated kidney injury-related biomarkers and immune-specific genes, thereby alleviating AKI in vivo. These findings suggest the potential use of HAase inhibitors for treating ischemic reperfusion-induced kidney injury.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206310","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":"Effects of <i>Ninjurin 2</i> polymorphisms on susceptibility to coronary heart disease.","authors":"Yuping Yan, Xiaoyan Du, Xia Dou, Jingjie Li, Wenjie Zhang, Shuangyu Yang, Wenting Meng, Gang Tian","doi":"10.1080/15384101.2024.2330225","DOIUrl":"10.1080/15384101.2024.2330225","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to explore the effects of Ninjurin 2 (NINJ2) polymorphisms on susceptibility to coronary heart disease (CHD).</p><p><strong>Methods: </strong>We conducted a case-control study with 499 CHD cases and 505 age and gender-matched controls. Five single nucleotide polymorphisms (SNPs) in NINJ2 (rs118050317, rs75750647, rs7307242, rs10849390, and rs11610368) were genotyped by the Agena MassARRAY platform. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression analysis to assess the association of NINJ2 polymorphisms and CHD risk-adjusted for age and gender. What's more, risk genes and molecular functions were screened via protein-protein interaction (PPI) network and functional enrichment analysis.</p><p><strong>Results: </strong>Rs118050317 in NINJ2 significantly increased CHD risk in people aged more than 60 years and women. Rs118050317 and rs7307242 had strong relationships with hypertension risk in CHD patients. Additionally, rs75750647 exceedingly raised diabetes risk in cases under multiple models, whereas rs10849390 could protect CHD patients from diabetes in allele, homozygote, and additive models. We also observed two blocks in NINJ2. Further interaction network and enrichment analysis showed that NINJ2 played a greater role in the pathogenesis and progression of CHD.</p><p><strong>Conclusion: </strong>Our results suggest that NINJ2 polymorphisms are associated with CHD risk.</p>","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140183887","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":"Correction.","authors":"","doi":"10.1080/15384101.2024.2317629","DOIUrl":"10.1080/15384101.2024.2317629","url":null,"abstract":"","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206309","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}