Pub Date : 2022-02-17DOI: 10.1016/j.stem.2022.02.004
Yanxin Li, Zhongqiu Li, Min Yang, Feiyang Wang, Yue Zhang, R. Li, Qian Li, Yunxia Gong, Binhong Wang, Baoguang Fan, Chunyue Wang, Lei Chen, Hong Li, Jennie Ong, Zhaoqian Teng, Lei Jin, Yan-Ling Wang, Peng Du, Jianwei Jiao
{"title":"Decoding the temporal and regional specification of microglia in the developing human brain.","authors":"Yanxin Li, Zhongqiu Li, Min Yang, Feiyang Wang, Yue Zhang, R. Li, Qian Li, Yunxia Gong, Binhong Wang, Baoguang Fan, Chunyue Wang, Lei Chen, Hong Li, Jennie Ong, Zhaoqian Teng, Lei Jin, Yan-Ling Wang, Peng Du, Jianwei Jiao","doi":"10.1016/j.stem.2022.02.004","DOIUrl":"https://doi.org/10.1016/j.stem.2022.02.004","url":null,"abstract":"","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49132148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lucia Capano, C. Sato, E. Ficulle, A. Yu, Kanta Horie, Ji-Sun Kwon, Kyle F. Burbach, Nicolas R. Barthélemy, Susan G. Fox, C. Karch, R. Bateman, H. Houlden, R. Morimoto, D. Holtzman, K. Duff, A. Yoo
Tau is a microtubule-binding protein expressed in neurons, and the equal ratios between 4-repeat (4R) and 3-repeat (3R) isoforms are maintained in normal adult brain function. Dysregulation of 3R:4R ratio causes tauopathy, and human neurons that recapitulate tau isoforms in health and disease will provide a platform for elucidating pathogenic processes involving tau pathology. We carried out extensive characterizations of tau isoforms expressed in human neurons derived by microRNA-induced neuronal reprogramming of adult fibroblasts. Transcript and protein analyses showed that miR neurons expressed all six isoforms with the 3R:4R isoform ratio equivalent to that detected in human adult brains. Also, miR neurons derived from familial tauopathy patients with a 3R:4R ratio altering mutation showed increased 4R tau and the formation of insoluble tau with seeding activity. Our results collectively demonstrate the utility of miRNA-induced neuronal reprogramming to recapitulate endogenous tau regulation comparable with the adult brain in health and disease.
{"title":"Recapitulation of endogenous 4R tau expression and formation of insoluble tau in directly reprogrammed human neurons.","authors":"Lucia Capano, C. Sato, E. Ficulle, A. Yu, Kanta Horie, Ji-Sun Kwon, Kyle F. Burbach, Nicolas R. Barthélemy, Susan G. Fox, C. Karch, R. Bateman, H. Houlden, R. Morimoto, D. Holtzman, K. Duff, A. Yoo","doi":"10.2139/ssrn.3899434","DOIUrl":"https://doi.org/10.2139/ssrn.3899434","url":null,"abstract":"Tau is a microtubule-binding protein expressed in neurons, and the equal ratios between 4-repeat (4R) and 3-repeat (3R) isoforms are maintained in normal adult brain function. Dysregulation of 3R:4R ratio causes tauopathy, and human neurons that recapitulate tau isoforms in health and disease will provide a platform for elucidating pathogenic processes involving tau pathology. We carried out extensive characterizations of tau isoforms expressed in human neurons derived by microRNA-induced neuronal reprogramming of adult fibroblasts. Transcript and protein analyses showed that miR neurons expressed all six isoforms with the 3R:4R isoform ratio equivalent to that detected in human adult brains. Also, miR neurons derived from familial tauopathy patients with a 3R:4R ratio altering mutation showed increased 4R tau and the formation of insoluble tau with seeding activity. Our results collectively demonstrate the utility of miRNA-induced neuronal reprogramming to recapitulate endogenous tau regulation comparable with the adult brain in health and disease.","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43600359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Akihiro Kaneshige, Takayuki Kaji, Lidan Zhang, Hayato Saito, Ayasa Nakamura, Tamaki Kurosawa, M. Ikemoto-Uezumi, K. Tsujikawa, S. Seno, M. Hori, Y. Saito, T. Matozaki, Kazumitsu Maehara, Y. Ohkawa, M. Potente, Shuichi Watanabe, T. Braun, A. Uezumi, S. Fukada
Adaptation to mechanical load, leading to enhanced force and power output, is a characteristic feature of skeletal muscle. Formation of new myonuclei required for efficient muscle hypertrophy relies on prior activation and proliferation of muscle stem cells (MuSCs). However, the mechanisms controlling MuSC expansion under conditions of increased load are not fully understood. Here we demonstrate that interstitial mesenchymal progenitors respond to mechanical load and stimulate MuSC proliferation in a surgical mouse model of increased muscle load. Mechanistically, transcriptional activation of Yes-associated protein 1 (Yap1)/transcriptional coactivator with PDZ-binding motif (Taz) in mesenchymal progenitors results in local production of thrombospondin-1 (Thbs1), which, in turn, drives MuSC proliferation through CD47 signaling. Under homeostatic conditions, however, CD47 signaling is insufficient to promote MuSC proliferation and instead depends on prior downregulation of the Calcitonin receptor. Our results suggest that relayed signaling between mesenchymal progenitors and MuSCs through a Yap1/Taz-Thbs1-CD47 pathway is critical to establish the supply of MuSCs during muscle hypertrophy.
{"title":"Relayed signaling between mesenchymal progenitors and muscle stem cells ensures adaptive stem cell response to increased mechanical load.","authors":"Akihiro Kaneshige, Takayuki Kaji, Lidan Zhang, Hayato Saito, Ayasa Nakamura, Tamaki Kurosawa, M. Ikemoto-Uezumi, K. Tsujikawa, S. Seno, M. Hori, Y. Saito, T. Matozaki, Kazumitsu Maehara, Y. Ohkawa, M. Potente, Shuichi Watanabe, T. Braun, A. Uezumi, S. Fukada","doi":"10.2139/ssrn.3815989","DOIUrl":"https://doi.org/10.2139/ssrn.3815989","url":null,"abstract":"Adaptation to mechanical load, leading to enhanced force and power output, is a characteristic feature of skeletal muscle. Formation of new myonuclei required for efficient muscle hypertrophy relies on prior activation and proliferation of muscle stem cells (MuSCs). However, the mechanisms controlling MuSC expansion under conditions of increased load are not fully understood. Here we demonstrate that interstitial mesenchymal progenitors respond to mechanical load and stimulate MuSC proliferation in a surgical mouse model of increased muscle load. Mechanistically, transcriptional activation of Yes-associated protein 1 (Yap1)/transcriptional coactivator with PDZ-binding motif (Taz) in mesenchymal progenitors results in local production of thrombospondin-1 (Thbs1), which, in turn, drives MuSC proliferation through CD47 signaling. Under homeostatic conditions, however, CD47 signaling is insufficient to promote MuSC proliferation and instead depends on prior downregulation of the Calcitonin receptor. Our results suggest that relayed signaling between mesenchymal progenitors and MuSCs through a Yap1/Taz-Thbs1-CD47 pathway is critical to establish the supply of MuSCs during muscle hypertrophy.","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45561212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-09-30DOI: 10.1101/2020.09.29.315713
K. Gowda, Derek Ping, Madhav Mani, S. Kuehn
The metabolic function of microbial communities has played a defining role in the evolution and persistence of life on Earth, driving redox reactions that form the basis of global biogeochemical cycles. Community metabolism emerges from a hierarchy of processes including gene expression, ecological interactions, and environmental factors. In wild communities, gene content is correlated with environmental context, but predicting metabolic dynamics from genomic structure remains elusive. Here we show, for the process of denitrification, that community metabolism is predictable from the genes each member of the community possesses. Machine learning reveals a sparse and generalizable mapping from gene content to metabolite dynamics across a genomically-diverse library of bacteria. A consumer-resource model correctly predicts community metabolism from single-strain phenotypes. Our results demonstrate that the conserved impacts of metabolic genes can predict community function, enabling the prediction of metabolite dynamics from metagenomes, designing denitrifying communities, and discovering how genome evolution impacts metabolism.
{"title":"Genomic structure predicts metabolite dynamics in microbial communities","authors":"K. Gowda, Derek Ping, Madhav Mani, S. Kuehn","doi":"10.1101/2020.09.29.315713","DOIUrl":"https://doi.org/10.1101/2020.09.29.315713","url":null,"abstract":"The metabolic function of microbial communities has played a defining role in the evolution and persistence of life on Earth, driving redox reactions that form the basis of global biogeochemical cycles. Community metabolism emerges from a hierarchy of processes including gene expression, ecological interactions, and environmental factors. In wild communities, gene content is correlated with environmental context, but predicting metabolic dynamics from genomic structure remains elusive. Here we show, for the process of denitrification, that community metabolism is predictable from the genes each member of the community possesses. Machine learning reveals a sparse and generalizable mapping from gene content to metabolite dynamics across a genomically-diverse library of bacteria. A consumer-resource model correctly predicts community metabolism from single-strain phenotypes. Our results demonstrate that the conserved impacts of metabolic genes can predict community function, enabling the prediction of metabolite dynamics from metagenomes, designing denitrifying communities, and discovering how genome evolution impacts metabolism.","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86608485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kitra Cates, M. McCoy, J. Kwon, Yangjian Liu, Daniel G. Abernathy, Bo Zhang, Shaopeng Liu, P. Gontarz, W. K. Kim, Shawei Chen, Wenjun Kong, Joshua N. Ho, Kyle F. Burbach, Harrison W. Gabel, Samantha A. Morris, A. Yoo
Cell-fate conversion generally requires reprogramming effectors to both introduce fate programs of the target cell type and erase the identity of starting cell population. Here, we reveal insights into the activity of microRNAs miR-9/9∗ and miR-124 (miR-9/9∗-124) as reprogramming agents that orchestrate direct conversion of human fibroblasts into motor neurons by first eradicating fibroblast identity and promoting uniform transition to a neuronal state in sequence. We identify KLF-family transcription factors as direct target genes for miR-9/9∗-124 and show their repression is critical for erasing fibroblast fate. Subsequent gain of neuronal identity requires upregulation of a small nuclear RNA, RN7SK, which induces accessibilities of chromatin regions and neuronal gene activation to push cells to a neuronal state. Our study defines deterministic components in the microRNA-mediated reprogramming cascade.
{"title":"Deconstructing Stepwise Fate Conversion of Human Fibroblasts to Neurons by MicroRNAs.","authors":"Kitra Cates, M. McCoy, J. Kwon, Yangjian Liu, Daniel G. Abernathy, Bo Zhang, Shaopeng Liu, P. Gontarz, W. K. Kim, Shawei Chen, Wenjun Kong, Joshua N. Ho, Kyle F. Burbach, Harrison W. Gabel, Samantha A. Morris, A. Yoo","doi":"10.2139/ssrn.3485473","DOIUrl":"https://doi.org/10.2139/ssrn.3485473","url":null,"abstract":"Cell-fate conversion generally requires reprogramming effectors to both introduce fate programs of the target cell type and erase the identity of starting cell population. Here, we reveal insights into the activity of microRNAs miR-9/9∗ and miR-124 (miR-9/9∗-124) as reprogramming agents that orchestrate direct conversion of human fibroblasts into motor neurons by first eradicating fibroblast identity and promoting uniform transition to a neuronal state in sequence. We identify KLF-family transcription factors as direct target genes for miR-9/9∗-124 and show their repression is critical for erasing fibroblast fate. Subsequent gain of neuronal identity requires upregulation of a small nuclear RNA, RN7SK, which induces accessibilities of chromatin regions and neuronal gene activation to push cells to a neuronal state. Our study defines deterministic components in the microRNA-mediated reprogramming cascade.","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48548224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-09-04DOI: 10.1101/2020.09.04.283218
Masaki Kinoshita, Michael Barber, William Mansfield, Yingzhi Cui, D. Spindlow, G. Stirparo, S. Dietmann, J. Nichols, Austin G Smith
Pluripotent cells emerge via a naïve founder population in the blastocyst, acquire capacity for germline and soma formation, and then undergo lineage priming. Mouse embryonic stem (ES) cells and epiblast stem cells (EpiSCs) represent the initial naïve and final primed phases of pluripotency, respectively. Here we investigate the intermediate formative stage. Using minimal exposure to specification cues, we expand stem cells from formative mouse epiblast. Unlike ES cells or EpiSCs, formative stem (FS) cells respond directly to germ cell induction. They colonise chimaeras including the germline. Transcriptome analyses show retained pre-gastrulation epiblast identity. Gain of signal responsiveness and chromatin accessibility relative to ES cells reflect lineage capacitation. FS cells show distinct transcription factor dependencies from EpiSCs, relying critically on Otx2. Finally, FS cell culture conditions applied to human naïve cells or embryos support expansion of similar stem cells, consistent with a conserved attractor state on the trajectory of mammalian pluripotency.
{"title":"Capture of Mouse and Human Stem Cells with Features of Formative Pluripotency","authors":"Masaki Kinoshita, Michael Barber, William Mansfield, Yingzhi Cui, D. Spindlow, G. Stirparo, S. Dietmann, J. Nichols, Austin G Smith","doi":"10.1101/2020.09.04.283218","DOIUrl":"https://doi.org/10.1101/2020.09.04.283218","url":null,"abstract":"Pluripotent cells emerge via a naïve founder population in the blastocyst, acquire capacity for germline and soma formation, and then undergo lineage priming. Mouse embryonic stem (ES) cells and epiblast stem cells (EpiSCs) represent the initial naïve and final primed phases of pluripotency, respectively. Here we investigate the intermediate formative stage. Using minimal exposure to specification cues, we expand stem cells from formative mouse epiblast. Unlike ES cells or EpiSCs, formative stem (FS) cells respond directly to germ cell induction. They colonise chimaeras including the germline. Transcriptome analyses show retained pre-gastrulation epiblast identity. Gain of signal responsiveness and chromatin accessibility relative to ES cells reflect lineage capacitation. FS cells show distinct transcription factor dependencies from EpiSCs, relying critically on Otx2. Finally, FS cell culture conditions applied to human naïve cells or embryos support expansion of similar stem cells, consistent with a conserved attractor state on the trajectory of mammalian pluripotency.","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43946090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-06-01DOI: 10.1016/j.stem.2020.05.012
Anonymous
{"title":"Stem Cell Research Responds to COVID-19: Deepak Srivastava, Fiona Watt, and George Daley","authors":"Anonymous","doi":"10.1016/j.stem.2020.05.012","DOIUrl":"https://doi.org/10.1016/j.stem.2020.05.012","url":null,"abstract":"","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.stem.2020.05.012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41376188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. Takayama, Alex Murison, Shin-ichiro Takayanagi, C. Arlidge, Stanley Zhou, Laura Garcia-Prat, Michelle A. Chan-Seng-Yue, Sasan Zandi, O. Gan, Helena Boutzen, K. Kaufmann, Aaron C Trotman-Grant, E. Schoof, Ken J. Kron, Noelia Díaz, John J. Y. Lee, T. Medina, D. D. De Carvalho, Michael D. Taylor, Juan M. Vaquerizas, Stephanie Z. Xie, J. Dick, M. Lupien
Lifelong blood production requires long-term hematopoietic stem cells (LT-HSCs), marked by stemness states involving quiescence and self-renewal, to transition into activated short-term HSCs (ST-HSCs) with reduced stemness. As few transcriptional changes underlie this transition, we used single-cell and bulk assay for transposase-accessible chromatin sequencing (ATAC-seq) on human HSCs and hematopoietic stem and progenitor cell (HSPC) subsets to uncover chromatin accessibility signatures, one including LT-HSCs (LT/HSPC signature) and another excluding LT-HSCs (activated HSPC [Act/HSPC] signature). These signatures inversely correlated during early hematopoietic commitment and differentiation. The Act/HSPC signature contains CCCTC-binding factor (CTCF) binding sites mediating 351 chromatin interactions engaged in ST-HSCs, but not LT-HSCs, enclosing multiple stemness pathway genes active in LT-HSCs and repressed in ST-HSCs. CTCF silencing derepressed stemness genes, restraining quiescent LT-HSCs from transitioning to activated ST-HSCs. Hence, 3D chromatin interactions centrally mediated by CTCF endow a gatekeeper function that governs the earliest fate transitions HSCs make by coordinating disparate stemness pathways linked to quiescence and self-renewal.
{"title":"The Transition from Quiescent to Activated States in Human Hematopoietic Stem Cells Is Governed by Dynamic 3D Genome Reorganization.","authors":"N. Takayama, Alex Murison, Shin-ichiro Takayanagi, C. Arlidge, Stanley Zhou, Laura Garcia-Prat, Michelle A. Chan-Seng-Yue, Sasan Zandi, O. Gan, Helena Boutzen, K. Kaufmann, Aaron C Trotman-Grant, E. Schoof, Ken J. Kron, Noelia Díaz, John J. Y. Lee, T. Medina, D. D. De Carvalho, Michael D. Taylor, Juan M. Vaquerizas, Stephanie Z. Xie, J. Dick, M. Lupien","doi":"10.2139/ssrn.3611286","DOIUrl":"https://doi.org/10.2139/ssrn.3611286","url":null,"abstract":"Lifelong blood production requires long-term hematopoietic stem cells (LT-HSCs), marked by stemness states involving quiescence and self-renewal, to transition into activated short-term HSCs (ST-HSCs) with reduced stemness. As few transcriptional changes underlie this transition, we used single-cell and bulk assay for transposase-accessible chromatin sequencing (ATAC-seq) on human HSCs and hematopoietic stem and progenitor cell (HSPC) subsets to uncover chromatin accessibility signatures, one including LT-HSCs (LT/HSPC signature) and another excluding LT-HSCs (activated HSPC [Act/HSPC] signature). These signatures inversely correlated during early hematopoietic commitment and differentiation. The Act/HSPC signature contains CCCTC-binding factor (CTCF) binding sites mediating 351 chromatin interactions engaged in ST-HSCs, but not LT-HSCs, enclosing multiple stemness pathway genes active in LT-HSCs and repressed in ST-HSCs. CTCF silencing derepressed stemness genes, restraining quiescent LT-HSCs from transitioning to activated ST-HSCs. Hence, 3D chromatin interactions centrally mediated by CTCF endow a gatekeeper function that governs the earliest fate transitions HSCs make by coordinating disparate stemness pathways linked to quiescence and self-renewal.","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49531655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-12-05DOI: 10.1016/j.stem.2019.11.006
P. Cannon
{"title":"Gene Editing Expands the Donor Pool for CCR5-Negative Stem Cell Transplants.","authors":"P. Cannon","doi":"10.1016/j.stem.2019.11.006","DOIUrl":"https://doi.org/10.1016/j.stem.2019.11.006","url":null,"abstract":"","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.stem.2019.11.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44933744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-12-05DOI: 10.1016/j.stem.2019.11.008
Valentina Scandella, M. Knobloch
{"title":"Sensing the Environment: Extracellular Lactate Levels Control Adult Neurogenesis.","authors":"Valentina Scandella, M. Knobloch","doi":"10.1016/j.stem.2019.11.008","DOIUrl":"https://doi.org/10.1016/j.stem.2019.11.008","url":null,"abstract":"","PeriodicalId":93928,"journal":{"name":"Cell stem cell","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.stem.2019.11.008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43089920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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