bioRxiv : the preprint server for biology最新文献

{"title":"Automated Classification of Sleep-Wake States and Seizures in Mice.","authors":"Brandon J Harvey, Viktor J Olah, Lauren M Aiani, Lucie I Rosenberg, Danny J Lasky, Benjamin Moxon, Nigel P Pedersen","doi":"10.1101/2023.04.07.536063","DOIUrl":"10.1101/2023.04.07.536063","url":null,"abstract":"<p><p>Sleep-wake states bi-directionally interact with epilepsy and seizures, but the mechanisms are unknown. A barrier to comprehensive characterization and the study of mechanisms has been the difficulty of annotating large chronic recording datasets. To overcome this barrier, we sought to develop an automated method of classifying sleep-wake states, seizures, and the post-ictal state in mice ranging from controls to mice with severe epilepsy with accompanying background EEG abnormalities. We utilized a large dataset of recordings, including EMG, EEG, and hippocampal local field potentials, from control and intra-amygdala kainic acid-treated mice. We found that an existing sleep-wake classifier performed poorly, even after retraining. A support vector machine, relying on typically used scoring parameters, also performed below our benchmark. We then trained and evaluated several multi-layer neural network architectures and found that a bidirectional long short-term memory-based model performed best. This 'Sleep-Wake and Ictal State Classifier' (SWISC) showed high agreement between ground-truth and classifier scores for all sleep and seizure states in an unseen and unlearned epileptic dataset (average agreement 96.41% ± SD 3.80%), and saline animals (97.77% ± 1.40%). Channel elimination and feature selection provided interpretability and demonstrated that SWISC was primarily dependent on hippocampal signals, yet still maintained good performance (∼90% agreement) with EEG alone, thereby expanding the classifier's applicability to other epilepsy datasets. SWISC enables the efficient combined scoring of sleep-wake and seizure states in mouse models of epilepsy and healthy controls, facilitating comprehensive and mechanistic studies of sleep-wake and biological rhythms in epilepsy.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0e/64/nihpp-2023.04.07.536063v1.PMC10104108.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9704206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CXCR6 promotes dermal CD8 ⁺ T cell survival and transition to long-term tissue residence.","authors":"Taylor A Heim, Ochapa Ibrahim, Ziyan Lin, Austin C Schultz, Maria M Steele, Tenny Mudianto, Amanda W Lund","doi":"10.1101/2023.02.14.528487","DOIUrl":"10.1101/2023.02.14.528487","url":null,"abstract":"<p><p>Tissue resident memory T cells (T _RM ) provide protection against local re-infection, and yet the interstitial signals necessary for their formation and persistence remain incompletely understood. Here we show that antigen-dependent induction of the chemokine receptor, CXCR6, is a conserved adaptation to peripheral tissue infiltration that promotes T _RM formation after viral infection. Deficient T _RM formation in the absence of CXCR6 was not explained by canonical trafficking as CXCR6 was not required for tissue entry, was dispensable for the early accumulation of antigen-specific CD8 ⁺ T cells in skin, and did not restrain their exit. Further, single cell sequencing indicated that <i>Cxcr6</i> ^-/- CD8 ⁺ T cells were competent to acquire a transcriptional program of residence and T _RM that formed were equally functional compared to their WT counterparts when reactivated greater than 100 days post primary infection. The reduced numbers observed at memory time points, where instead found to associate with impaired redox homeostasis and antioxidant capacity during the transition from effector to memory states. As such, <i>Cxcr6</i> ^-/- CD8 ⁺ T cells exhibited increased rates of apoptosis in the dermis relative to controls, which led to reduced numbers of T _RM in the epidermis at memory. CXCR6 therefore promotes the metabolic adaptation of T cells as they engage antigen in tissue to increase the probability of memory differentiation and long-term residence.</p><p><strong>One sentence summary: </strong>CXCR6 promotes mechanisms of cellular adaptation to tissue that support local survival and the transition to tissue residence.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/cd/b3/nihpp-2023.02.14.528487v1.PMC9949075.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9073967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The striatal heterogeneous nuclear ribonucleoprotein H mRNA targetome associated with methamphetamine administration and behavior.","authors":"Qiu T Ruan, William B Lynch, Rebecca H Cole, Michael A Rieger, Britahny M Baskin, Sophia A Miracle, Jacob A Beierle, Emily J Yao, Jiayi W Cox, Amarpreet Kandola, Kayla T Richardson, Melanie M Chen, Julia C Kelliher, R Keith Babbs, Peter E A Ash, Benjamin Wolozin, Karen K Szumlinski, W Evan Johnson, Joseph D Dougherty, Camron D Bryant","doi":"10.1101/2021.07.06.451358","DOIUrl":"10.1101/2021.07.06.451358","url":null,"abstract":"<p><p>Methamphetamine addiction remains a major public health concern in the United States that has paralleled the opioid epidemic. Psychostimulant use disorders have a heritable genetic component that remains unexplained. Methamphetamine targets membrane and vesicular transporters to increase synaptic dopamine, norepinephrine, and serotonin. We previously identified <i>Hnrnph1</i> (heterogeneous nuclear ribonucleoprotein H1) as a quantitative trait gene underlying methamphetamine behavioral sensitivity. <i>Hnrnph1</i> encodes the RNA-binding protein hnRNP H1 that is ubiquitously expressed in neurons throughout the brain. Gene-edited mice with a heterozygous frameshift deletion in <i>Hnrnph1's</i> first coding exon of showed reduced methamphetamine-induced dopamine release and behaviors. To inform the mechanism linking hnRNP H with methamphetamine neurobehavioral effects, we surveyed the mRNA targetome of hnRNP H via cross-linking immunoprecipitation coupled with RNA-sequencing in striatal tissue at baseline and at 30 min post-methamphetamine in wild-type male and female C57BL/6J mice. Methamphetamine induced changes in RNA-binding targets of hnRNP H in mice, including differential binding to 3'UTR targets and multiple enriched mRNAs involved in synaptic plasticity. Targetome, transcriptome, and spliceome analyses triangulated on <i>Cacna2d2</i> as a suggestive target, with differences in hnRNP H binding, gene expression and splicing following methamphetamine treatment (2 mg/kg, i.p.). Furthermore, pre-treatment with pregabalin, an inhibitor of α2δ2 and α2δ1 voltage-gated calcium channel subunits, attenuated methamphetamine-induced locomotor activity in male and female mice, supporting a role for Cacna2d1/d2 in methamphetamine locomotor stimulant sensitivity. Our study identifies a dynamic hnRNP H RNA targetome that can rapidly and adaptively respond to methamphetamine to regulate gene expression and likely synaptic plasticity and behavior.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12154668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82387600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rab10 inactivation promotes AMPAR trafficking and spine enlargement during long-term potentiation.","authors":"Jie Wang, Jun Nishiyama, Paula Parra-Bueno, Elwy Okaz, Goksu Oz, Xiaodan Liu, Tetsuya Watabe, Irena Suponitsky-Kroyter, Timothy E McGraw, Erzsebet M Szatmari, Ryohei Yasuda","doi":"10.1101/2022.05.17.492345","DOIUrl":"10.1101/2022.05.17.492345","url":null,"abstract":"<p><p>Rab-dependent membrane trafficking is critical for changing the structure and function of dendritic spines during synaptic plasticity. Here, we developed highly sensitive sensors to monitor Rab protein activity in single dendritic spines undergoing structural long-term potentiation (sLTP) in rodent organotypic hippocampal slices. During sLTP, Rab10 was persistently inactivated (>30 min) in the stimulated spines, whereas Rab4 was transiently activated over ~5 min. Inhibiting or deleting Rab10 enhanced sLTP, electrophysiological LTP and AMPA receptor (AMPAR) trafficking during sLTP. In contrast, disrupting Rab4 impaired sLTP only in the first few minutes, and decreased AMPAR trafficking during sLTP. Thus, our results suggest that Rab10 and Rab4 oppositely regulate AMPAR trafficking during sLTP, and inactivation of Rab10 signaling facilitates the induction of LTP and associated spine structural plasticity.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12154598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79706128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging reduces the number and function of L-type calcium channels in the membrane of cardiac pacemaker cells.","authors":"Oscar Vivas, Matthias Baudot, Roxanne Madden, Sabrina Choi, Victor A Flores, L Fernando Santana, Claudia M Moreno","doi":"10.1101/2022.06.22.497267","DOIUrl":"10.1101/2022.06.22.497267","url":null,"abstract":"<p><p>Every heartbeat is initiated by a spontaneous electrical signal generated inside the cardiac pacemaker. The generation of this electrical signal depends on the coordinated opening and closing of different ion channels, where voltage-gated L-type calcium channels play a central role. Despite the reliability of the pacemaker, all mammals experience a linear slowdown of the pacemaker rate with age. In humans, this slowing can become pathological and constitutes the main cause for the requirement of the implantation of artificial pacemakers. However, the mechanisms behind the age-associated slowdown of the pacemaker are not well understood. Here, we show that age alters L-type calcium channels in pacemaker cells from mice. The age-associated alterations include: i) a reduction in the density of the channels at the plasma membrane, ii) a reduction in the clustering of the channels, and iii) a decrease in channel open probability. Altogether, these age-associated alterations result in a global reduction of the L-type calcium current density and in a slowdown of the pacemaker diastolic depolarization. Remarkably, increasing the open probability of L-type calcium channels pharmacologically was enough to restore pacemaker rate in old cells to the same levels observed in the young. Overall, our findings provide evidence that proper organization and function of L-type calcium channels is impaired by aging and that this dysfunction contributes to the slowdown of pacemaker cells in old animals.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"174 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12154664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80728210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WITHDRAWN: Cell based dATP delivery as a therapy for chronic heart failure.","authors":"Ketaki N Mhatre, Julie Mathieu, Amy Martinson, Galina Flint, Leslie P Blakley, Arash Tabesh, Hans Reinecke, Xiulan Yang, Xuan Guan, Eesha Murali, Jordan M Klaiman, Guy L Odom, Mary Beth Brown, Rong Tian, Stephen D Hauschka, Daniel Raftery, Farid Moussavi-Harami, Michael Regnier, Charles E Murry","doi":"10.1101/2023.04.24.538108","DOIUrl":"10.1101/2023.04.24.538108","url":null,"abstract":"<p><p>The authors have withdrawn this manuscript because the senior authors have identified inconsistencies in the data presented in this manuscript, which affect the reliability of the main conclusions. In keeping with our commitment to scientific rigor and transparency, the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding authors.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f9/64/nihpp-2023.04.24.538108v1.PMC10168250.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10166045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacteria detect neutrophils via a system that responds to hypochlorous acid and flow.","authors":"Ilona P Foik, Runhang Shu, Serena Abbondante, Summer J Kasallis, Lauren A Urban, Andy P Huang, Leora Duong, Michaela E Marshall, Eric Pearlman, Timothy L Downing, Albert Siryaporn","doi":"10.1101/2022.02.01.478687","DOIUrl":"10.1101/2022.02.01.478687","url":null,"abstract":"<p><p>Neutrophils respond to the presence of bacteria by producing oxidative molecules that are lethal to bacteria, including hypochlorous acid (HOCl). However, the extent to which bacteria detect activated neutrophils or the HOCl that neutrophils produce, has not been understood. Here we report that the opportunistic bacterial pathogen <i>Pseudomonas aeruginosa</i> upregulates expression of its <i>fro</i> operon in response to stimulated neutrophils. This operon was previously shown to be activated by shear rate of fluid flow in the environment. We show that <i>fro</i> is specifically upregulated by HOCl, while other oxidative factors that neutrophils produce including H₂O₂, do not upregulate <i>fro</i>. The <i>fro</i>-dependent response to HOCl upregulates the expression of multiple methionine sulfoxide reductases, which relieve oxidative stress that would otherwise inhibit growth. Our findings suggest a model in which the detection of shear rate or HOCl activates the <i>fro</i> operon, which serves as an early and sensitive host-detection system for <i>P. aeruginosa</i> that improves its own survival against neutrophil-mediated host defenses. In support of this model, we found that the <i>fro</i> operon is activated in an infection model where flow and neutrophils are present. This response could promote the bacterium's pathogenicity, colonization of tissue, and persistence in infections.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82540699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional genomic analysis of non-canonical DNA regulatory elements of the aryl hydrocarbon receptor.","authors":"Shayan Shahriar, Tajhal D Patel, Manjula Nakka, Sandra L Grimm, Cristian Coarfa, Daniel A Gorelick","doi":"10.1101/2023.05.01.538985","DOIUrl":"10.1101/2023.05.01.538985","url":null,"abstract":"<p><p>The aryl hydrocarbon receptor (AHR) is a ligand-dependent transcription factor that is activated by environmental toxicants, like halogenated and polycyclic aromatic hydrocarbons, and then binds to DNA and regulates gene expression. AHR is involved in various physiological processes, including liver and immune system function, cell cycle regulation, oncogenesis, and metabolism. In the canonical pathway, AHR binds to a consensus DNA sequence (GCGTC), termed the xenobiotic response element (XRE), recruits protein coregulators, and regulates target gene expression. Emerging evidence suggests that AHR may regulate gene expression via an additional pathway, by binding to a non-consensus DNA sequence (GGGA) termed the non- consensus XRE (NC-XRE). The prevalence of NC-XRE motifs in the genome is not known. Studies using chromatin immunoprecipitation and reporter genes provide indirect evidence of AHR-NC-XRE interactions, but direct evidence for an AHR-NC-XRE interaction that regulates transcription in a natural genomic context is lacking. Here, we analyzed AHR binding to NC-XRE DNA on a genome-wide scale in mouse liver. We integrated ChIP-seq and RNA-seq data and identified putative AHR target genes with NC-XRE motifs in regulatory regions. We found that NC-XRE motifs are present in 82% of AHR-bound DNA, which are significantly enriched relative to random genomic regions. These AHR-bound regions include, but are not limited to, promoters and enhancers of AHR target genes. To obtain direct evidence of AHR regulation via this non-canonical pathway, we performed functional genomics on the mouse <i>Serpine1</i> gene, a putative AHR target via NC-XRE. Deleting NC-XRE motifs from the <i>Serpine1</i> promoter reduced the upregulation of <i>Serpine1</i> by TCDD, an AHR ligand. We conclude that AHR upregulates <i>Serpine1</i> via NC-XRE DNA. Taken together, our results provide the first direct evidence of AHR-mediated gene regulation via NC-XRE in a natural genomic context. These findings enhance our understanding of AHR-bound DNA regions and their influence on target gene expression. Our results will also improve our ability to identify AHR target genes and their physiological relevance.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/26/49/nihpp-2023.05.01.538985v1.PMC10187216.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10425783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Mediator Kinase Module regulates cell cycle re-entry and transcriptional responses following DNA damage.","authors":"Gönen Memişoğlu, Stefan Bohn, Nevan J Krogan, James E Haber, Alexander J Ruthenburg","doi":"10.1101/2023.02.26.530133","DOIUrl":"10.1101/2023.02.26.530133","url":null,"abstract":"<p><p>The Cdk8 kinase module (CKM) is a non-obligate and dissociable subcomplex of Mediator of transcription, a key regulator of RNA polymerase II (RNAPII). Through a genetic screen in yeast, we discovered a surprising role for Mediator CKM in the DNA damage response (DDR) and mitotic re-entry. Remarkably, we find that a single DNA break is sufficient for CKM-dependent global transcriptional attenuation. Upon DDR activation, the kinase activity of CKM antagonizes RNAPII binding to core Mediator, thereby reducing the transcriptionally-engaged RNAPII pool. This transcriptional attenuation is essential for DDR inactivation and limits the spreading of γ-H2AX into gene bodies. Furthermore, CKM localizes to DNA breaks to impede RNAPII binding. Importantly, we demonstrate that the role of CKM on DDR and transcriptional attenuation is conserved from yeast to mammals, establishing a multifaceted and essential function for CKM in transcriptional regulation of DNA-damage response.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77839067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vivo CRISPR screening identifies SAGA complex members as key regulators of hematopoiesis.","authors":"Michael S Haney, Archana Shankar, Leonid Olender, Ian Hsu, Masashi Miyauchi, Róbert Pálovics, Grace A Meaker, Satoshi Kaito, Ola Rizq, Hwei Minn Khoo, Yavor Bozhilov, Kyomi J Igarashi, Joydeep Bhadury, Christy Munson, Paul K Mack, Tze-Kai Tan, Jan Rehwinkel, Atushi Iwama, Tony Wyss-Coray, Hiromitsu Nakauchi, Adam C Wilkinson","doi":"10.1101/2022.07.22.501030","DOIUrl":"10.1101/2022.07.22.501030","url":null,"abstract":"<p><p>The biological mechanisms that sustain the vast blood production required for healthy life remain incompletely understood. To search for novel regulators of hematopoiesis, we performed genome-wide in vivo hematopoietic stem cell (HSC)-based CRISPR knockout screens for regulators of hematopoiesis. We discovered SAGA complex members, including <i>Tada2b</i> and <i>Taf5l</i> , as key regulators of hematopoiesis. Loss of <i>Tada2b</i> or <i>Taf5l</i> strongly inhibited hematopoiesis <i>in vivo</i> , led to a buildup of immature hematopoietic cells in the bone marrow, and was associated with upregulation of interferon pathway genes. Loss of these factors also enhanced the cell outgrowth and the interferon pathway in an <i>in vivo</i> human myelodysplastic syndrome model, suggesting that loss of SAGA complex activity could contribute to hematological disease progression. In summary, this study has identified the SAGA complex as an important regulator of hematopoiesis.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"2018 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87799153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}