CoChat
Sign Up
Cited by 28Neurogenesis and neuroplasticity mechanismsDevelopmental Biology and Gene RegulationAutophagy in Disease and Therapy

Lysosomes and signaling pathways for maintenance of quiescence in adult neural stem cells

Open access
Kobayashi, Taeko, Kageyama, Ryoichiro·2021·The FEBS Journal
DOI 10.1111/febs.15555PMC PMC8246936
Open this paper in CoChat — free accountOpen PDF

Abstract

Quiescence is a cellular strategy for maintaining somatic stem cells in a specific niche in a low metabolic state without senescence for a long period of time. During development, neural stem cells (NSCs) actively proliferate and self‐renew, and their progeny differentiate into both neurons and glial cells to form mature brain tissues. On the other hand, most NSCs in the adult brain are quiescent and arrested in G0/G1 phase of the cell cycle. Quiescence is essential in order to avoid the precocious exhaustion of NSCs, ensuring a sustainable source of available stem cells in the brain throughout the lifespan. After receiving activation signals, quiescent NSCs reenter the cell cycle and generate new neurons. This switching between quiescence and proliferation is tightly regulated by diverse signaling pathways. Recent studies suggest significant involvement of cellular proteostasis (homeostasis of the proteome) in the quiescent state of NSCs. Proteostasis is the result of integrated regulation of protein synthesis, folding, and degradation. In this review, we discuss regulation of quiescence by multiple signaling pathways, especially bone morphogenetic protein and Notch signaling, and focus on the functional involvement of the lysosome, an organelle governing cellular degradation, in quiescence of adult NSCs.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1111/febs.15555

Cites

15 of 15 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • As more genome-wide association studies and familial cohort sequencing studies have been performed, many additional risk and rare causative alleles have been found.

    “As more genome-wide association studies (GWAS) and familial cohort sequencing studies have been performed, many additional risk and rare causative alleles have been found.88”

    From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [88]

    The closest body-text passage, in “Lysosomes in quiescent NSCs” (page unavailable), discusses autophagy and neural stem cells, not the discovery of risk or rare causative alleles. Searches for GWAS, familial sequencing, and rare causative alleles found no passage in our copy addressing the claim. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

  • Mutations in cathepsins D and F lead to NCL.

    “Mutations in several of the cathepsins lead to NCL (D and F), and others have also been identified as risk factors for neurodegenerative disease (B, D, and F).88,122,123”

    From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [88]

    The 'Lysosomes in quiescent NSCs' section discusses lysosomal activity and autophagy, but does not address cathepsin D or F mutations or NCL. Searches for those terms and for cathepsins in neurodegenerative disease found no passage in our copy supporting the claim; no page numbers were provided. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

  • Cathepsins B, D, and F are risk factors for neurodegenerative disease.

    “Mutations in several of the cathepsins lead to NCL (D and F), and others have also been identified as risk factors for neurodegenerative disease (B, D, and F).88,122,123”

    From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [88]

    The section “The lysosome: a digestive organelle and a hub of nutrition signaling” describes lysosomal degradation, and “Lysosomes in quiescent NSCs” discusses autophagy and neural stem cells; neither identifies cathepsins B, D, or F as neurodegenerative-disease risk factors. Searches for cathepsin, neuronal ceroid lipofuscinosis, and the risk-factor claim found no passage addressing that association. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 74

  1. [1]Altman J & Das GD (1965) Autoradiographic and histological evidence of postnatal hippocampal neurogenesis in rats. J Comp Neur 124, 319– 336. 5861717
  2. [2]Doetsch F, Caille I, Lim DA, Garcia‐Verdugo JM & Alvarez‐Buylla A (1999) Subventricular zone astrocytes are neural stem cells in the adult mammalian brain. Cell 97, 703– 716. 10380923
  3. [3]Eriksson PS, Perfilieva E, Björk‐Eriksson T, Alborn M, Nordborg C, Peterson DA & Gage FH (1998) Neurogenesis in the adult human hippocampus. Nat Med 4, 1313– 1317. 9809557
  4. [5]Lim DA & Alvarez‐Buylla A (2016) The adult ventricular‐subventricular zone (V‐SVZ) and olfactory bulb (OB) neurogenesis. Cold Spring Harb Perspect Biol 8, a018820. 27048191 PMC4852803
  5. [6]Urban N, Blomfield IM & Guillemot F (2019) Quiescence of adult mammalian neural stem cells: a highly regulated rest. Neuron 104, 834– 848. 31805262
  6. [8]Martynoga B, Mateo JL, Zhou B, Andersen J, Achimastou A, Urban N, van den Berg D, Georgopoulou D, Hadjur S, Wittbrodt J et al. (2013) Epigenomic enhancer annotation reveals a key role for NFIX in neural stem cell quiescence. Genes Dev 27, 1769– 1786. 23964093 PMC3759694
  7. [9]Urban N, van den Berg DL, Forget A, Andersen J, Demmers JA, Hunt C, Ayrault O & Guillemot F (2016) Return to quiescence of mouse neural stem cells by degradation of a proactivation protein. Science 353, 292– 295. 27418510 PMC5321528
  8. [10]Balch WE, Morimoto RI, Dillin A & Kelly JW (2008) Adapting proteostasis for disease intervention. Science 319, 916– 919. 18276881
  9. [11]Joppe SE, Hamilton LK, Cochard LM, Levros LC, Aumont A, Barnabe‐Heider F & Fernandes KJ (2015) Bone morphogenetic protein dominantly suppresses epidermal growth factor‐induced proliferative expansion of adult forebrain neural precursors. Front Neurosci 9, 407. 26576147 PMC4625077
  10. [13]Lim DA, Tramontin AD, Trevejo JM, Herrera DG, García‐Verdugo JM & Alvarez‐Buylla A (2000) Noggin antagonizes BMP signaling to create a niche for adult neurogenesis. Neuron 28, 713– 726. 11163261
  11. [14]Colak D, Mori T, Brill MS, Pfeifer A, Falk S, Deng C, Monteiro R, Mummery C, Sommer L & Gotz M (2008) Adult neurogenesis requires Smad4‐mediated bone morphogenic protein signaling in stem cells. J Neurosci 28, 434– 446. 18184786 PMC6670509
  12. [15]Bonaguidi MA, Peng CY, McGuire T, Falciglia G, Gobeske KT, Czeisler C & Kessler JA (2008) Noggin expands neural stem cells in the adult hippocampus. J Neurosci 28, 9194– 9204. 18784300 PMC3651371
  13. [16]Peretto P, Dati C, De Marchis S, Kim HH, Ukhanova M, Fasolo A & Margolis FL (2004) Expression of the secreted factors noggin and bone morphogenetic proteins in the subependymal layer and olfactory bulb of the adult mouse brain. Neuroscience 128, 685– 696. 15464277
  14. [18]Wegleiter T, Buthey K, Gonzalez‐Bohorquez D, Hruzova M, Bin Imtiaz MK, Abegg A, Mebert I, Molteni A, Kollegger D, Pelczar P et al. (2019) Palmitoylation of BMPR1a regulates neural stem cell fate. Proc Natl Acad Sci USA 116, 25688– 25696. 31772009 PMC6926058
  15. [19]Yousef H, Morgenthaler A, Schlesinger C, Bugaj L, Conboy IM & Schaffer DV (2015) Age‐associated increase in BMP signaling inhibits hippocampal neurogenesis. Stem Cells 33, 1577– 1588. 25538007 PMC4818000
  16. [20]Kageyama R, Ohtsuka T & Kobayashi T (2007) The Hes gene family: repressors and oscillators that orchestrate embryogenesis. Development 134, 1243– 1251. 17329370
  17. [21]Irvin DK, Zurcher SD, Nguyen T, Weinmaster G & Kornblum HI (2001) Expression patterns of Notch1, Notch2, and Notch3 suggest multiple functional roles for the notch‐DSL signaling system during brain development. J Comp Neurol 436, 167– 181. 11438922
  18. [22]Giachino C, Basak O, Lugert S, Knuckles P, Obernier K, Fiorelli R, Frank S, Raineteau O, Alvarez‐Buylla A & Taylor V (2014) Molecular diversity subdivides the adult forebrain neural stem cell population. Stem Cells 32, 70– 84. 23964022 PMC4259462
  19. [23]Lugert S, Basak O, Knuckles P, Haussler U, Fabel K, Götz M, Haas CA, Kempermann G, Taylor V & Giachino C (2010) Quiescent and active hippocampal neural stem cells with distinct morphologies respond selectively to physiological and pathological stimuli and aging. Cell Stem Cell 6, 445– 456. 20452319
  20. [24]Ehm O, Goritz C, Covic M, Schaffner I, Schwarz TJ, Karaca E, Kempkes B, Kremmer E, Pfrieger FW, Espinosa L et al. (2010) RBPJkappa‐dependent signaling is essential for long‐term maintenance of neural stem cells in the adult hippocampus. J Neurosci 30, 13794– 13807. 20943920 PMC6633732
  21. [26]Engler A, Rolando C, Giachino C, Saotome I, Erni A, Brien C, Zhang R, Zimber‐Strobl U, Radtke F, Artavanis‐Tsakonas S et al. (2018) Notch2 signaling maintains NSC quiescence in the murine ventricular‐subventricular zone. Cell Rep 22, 992– 1002. 29386140
  22. [27]Ables JL, Decarolis NA, Johnson MA, Rivera PD, Gao Z, Cooper DC, Radtke F, Hsieh J & Eisch AJ (2010) Notch1 is required for maintenance of the reservoir of adult hippocampal stem cells. J Neurosci 30, 10484– 10492. 20685991 PMC2935844
  23. [28]Breunig JJ, Silbereis J, Vaccarino FM, Sestan N & Rakic P (2007) Notch regulates cell fate and dendrite morphology of newborn neurons in the postnatal dentate gyrus. Proc Natl Acad Sci USA 104, 20558– 20563. 18077357 PMC2154470
  24. [29]Basak O, Giachino C, Fiorini E, Macdonald HR & Taylor V (2012) Neurogenic subventricular zone stem/progenitor cells are Notch1‐dependent in their active but not quiescent state. J Neurosci 32, 5654– 5666. 22514327 PMC6703480
  25. [30]Zhang R, Boareto M, Engler A, Louvi A, Giachino C, Iber D & Taylor V (2019) Id4 downstream of Notch2 maintains neural stem cell quiescence in the adult hippocampus. Cell Rep 28, 1485– 1498.e6. 31390563
  26. [32]Ehret F, Vogler S, Pojar S, Elliott DA, Bradke F, Steiner B & Kempermann G (2015) Mouse model of CADASIL reveals novel insights into Notch3 function in adult hippocampal neurogenesis. Neurobiol Dis 75, 131– 141. 25555543
  27. [33]Wang LH & Baker NE (2015) E proteins and ID proteins: helix‐loop‐helix partners in development and disease. Dev Cell 35, 269– 380. 26555048 PMC4684411
  28. [34]Blomfield IM, Rocamonde B, Masdeu MDM, Mulugeta E, Vaga S, van den Berg DL, Huillard E, Guillemot F & Urban N (2019) Id4 promotes the elimination of the pro‐activation factor Ascl1 to maintain quiescence of adult hippocampal stem cells. Elife 8, e48561. 31552825 PMC6805120
  29. [35]Sueda R, Imayoshi I, Harima Y & Kageyama R (2019) High Hes1 expression and resultant Ascl1 suppression regulate quiescent vs. active neural stem cells in the adult mouse brain. Genes Dev 33, 511– 523. 30862661 PMC6499325
  30. [36]Shimojo H, Ohtsuka T & Kageyama R (2008) Oscillations in notch signaling regulate maintenance of neural progenitors. Neuron 58, 52– 64. 18400163
  31. [37]Imayoshi I, Isomura A, Harima Y, Kawaguchi K, Kori H, Miyachi H, Fujiwara T, Ishidate F & Kageyama R (2013) Oscillatory control of factors determining multipotency and fate in mouse neural progenitors. Science 342, 1203– 1208. 24179156
  32. [38]Alfonso J, Le Magueresse C, Zuccotti A, Khodosevich K & Monyer H (2012) Diazepam binding inhibitor promotes progenitor proliferation in the postnatal SVZ by reducing GABA signaling. Cell Stem Cell 10, 76– 87. 22226357
  33. [39]Song J, Zhong C, Bonaguidi MA, Sun GJ, Hsu D, Gu Y, Meletis K, Huang ZJ, Ge S, Enikolopov G et al. (2012) Neuronal circuitry mechanism regulating adult quiescent neural stem‐cell fate decision. Nature 489, 150– 154. 22842902 PMC3438284
  34. [40]Zhou Y, Bond AM, Shade JE, Zhu Y, Davis CO, Wang X, Su Y, Yoon KJ, Phan AT, Chen WJ et al. (2018) Autocrine Mfge8 signaling prevents developmental exhaustion of the adult neural stem cell pool. Cell Stem Cell 23, 444– 452.e4. 30174295 PMC6128767
  35. [41]Liu X, Wang Q, Haydar TF & Bordey A (2005) Nonsynaptic GABA signaling in postnatal subventricular zone controls proliferation of GFAP‐expressing progenitors. Nat Neurosci 8, 1179– 1187. 16116450 PMC1380263
  36. [42]Delgado AC, Ferron SR, Vicente D, Porlan E, Perez‐Villalba A, Trujillo CM, D'Ocon P & Farinas I (2014) Endothelial NT‐3 delivered by vasculature and CSF promotes quiescence of subependymal neural stem cells through nitric oxide induction. Neuron 83, 572– 585. 25043422
  37. [43]Ballabio A & Bonifacino JS (2020) Lysosomes as dynamic regulators of cell and organismal homeostasis. Nat Rev Mol Cell Biol 21, 101– 118. 31768005
  38. [44]Holland LKK, Nielsen IO, Maeda K & Jaattela M (2020) SnapShot: lysosomal functions. Cell 181, 748.e1. 32359442
  39. [45]Sancak Y, Bar‐Peled L, Zoncu R, Markhard AL, Nada S & Sabatini DM (2010) Ragulator‐Rag complex targets mTORC1 to the lysosomal surface and is necessary for its activation by amino acids. Cell 141, 290– 303. 20381137 PMC3024592
  40. [46]Pena‐Llopis S, Vega‐Rubin‐de‐Celis S, Schwartz JC, Wolff NC, Tran TA, Zou L, Xie XJ, Corey DR & Brugarolas J (2011) Regulation of TFEB and V‐ATPases by mTORC1. EMBO J 30, 3242– 3258. 21804531 PMC3160667
  41. [47]Settembre C, Zoncu R, Medina DL, Vetrini F, Erdin S, Erdin S, Huynh T, Ferron M, Karsenty G, Vellard MC et al. (2012) A lysosome‐to‐nucleus signalling mechanism senses and regulates the lysosome via mTOR and TFEB. EMBO J 31, 1095– 1108. 22343943 PMC3298007
  42. [48]Steingrimsson E, Tessarollo L, Reid SW, Jenkins NA & Copeland NG (1998) The bHLH‐Zip transcription factor Tfeb is essential for placental vascularization. Development 125, 4607– 4616. 9806910
  43. [49]Sardiello M, Palmieri M, di Ronza A, Medina DL, Valenza M, Gennarino VA, Di Malta C, Donaudy F, Embrione V, Polishchuk RS et al. (2009) A gene network regulating lysosomal biogenesis and function. Science 325, 473– 477. 19556463
  44. [50]Medina DL, Fraldi A, Bouche V, Annunziata F, Mansueto G, Spampanato C, Puri C, Pignata A, Martina JA, Sardiello M et al. (2011) Transcriptional activation of lysosomal exocytosis promotes cellular clearance. Dev Cell 21, 421– 430. 21889421 PMC3173716
  45. [51]Miao R, Li M, Zhang Q, Yang C & Wang X (2020) An ECM‐to‐nucleus signaling pathway activates lysosomes for C. elegans larval development. Dev Cell 52, 21– 37 e5. 31735670
  46. [52]Thelen AM & Zoncu R (2017) Emerging roles for the lysosome in lipid metabolism. Trends Cell Biol 27, 833– 850. 28838620 PMC5653458
  47. [53]Li P, Gu M & Xu H (2019) Lysosomal ion channels as decoders of cellular signals. Trends Biochem Sci 44, 110– 124. 30424907 PMC6340733
  48. [55]Hartl FU, Bracher A & Hayer‐Hartl M (2011) Molecular chaperones in protein folding and proteostasis. Nature 475, 324– 332. 21776078
  49. [56]Leeman DS, Hebestreit K, Ruetz T, Webb AE, McKay A, Pollina EA, Dulken BW, Zhao X, Yeo RW, Ho TT et al. (2018) Lysosome activation clears aggregates and enhances quiescent neural stem cell activation during aging. Science 359, 1277– 1283. 29590078 PMC5915358
  50. [57]Kobayashi T, Piao W, Takamura T, Kori H, Miyachi H, Kitano S, Iwamoto Y, Yamada M, Imayoshi I, Shioda S et al. (2019) Enhanced lysosomal degradation maintains the quiescent state of neural stem cells. Nat Commun 10, 5446. 31784517 PMC6884460
  51. [58]Morrow CS, Porter TJ, Xu N, Arndt ZP, Ako‐Asare K, Heo HJ, Thompson EAN & Moore DL (2020) Vimentin coordinates protein turnover at the aggresome during neural stem cell quiescence exit. Cell Stem Cell 26, 558– 568.e9. 32109376 PMC7127969
  52. [59]Laporte D, Salin B, Daignan‐Fornier B & Sagot I (2008) Reversible cytoplasmic localization of the proteasome in quiescent yeast cells. J Cell Biol 181, 737– 745. 18504300 PMC2396804
  53. [60]Kalamakis G, Brune D, Ravichandran S, Bolz J, Fan W, Ziebell F, Stiehl T, Catala‐Martinez F, Kupke J, Zhao S et al. (2019) Quiescence modulates stem cell maintenance and regenerative capacity in the aging brain. Cell 176, 1407– 1419.e14. 30827680
  54. [62]Shen HM & Mizushima N (2014) At the end of the autophagic road: an emerging understanding of lysosomal functions in autophagy. Trends Biochem Sci 39, 61– 71. 24369758
  55. [64]Xi Y, Dhaliwal JS, Ceizar M, Vaculik M, Kumar KL & Lagace DC (2016) Knockout of Atg5 delays the maturation and reduces the survival of adult‐generated neurons in the hippocampus. Cell Death Dis 7, e2127. PMC4823925 26938300
  56. [65]Wu X, Fleming A, Ricketts T, Pavel M, Virgin H, Menzies FM & Rubinsztein DC (2016) Autophagy regulates Notch degradation and modulates stem cell development and neurogenesis. Nat Commun 7, 10533. 26837467 PMC4742842
  57. [66]Yazdankhah M, Farioli‐Vecchioli S, Tonchev AB, Stoykova A & Cecconi F (2014) The autophagy regulators Ambra1 and Beclin 1 are required for adult neurogenesis in the brain subventricular zone. Cell Death Dis 5, e1403. 25188513 PMC4540193
  58. [67]Petri R, Pircs K, Jonsson ME, Akerblom M, Brattas PL, Klussendorf T & Jakobsson J (2017) let‐7 regulates radial migration of new‐born neurons through positive regulation of autophagy. EMBO J 36, 1379– 1391. 28336683 PMC5430214
  59. [68]Paik JH, Ding Z, Narurkar R, Ramkissoon S, Muller F, Kamoun WS, Chae SS, Zheng H, Ying H, Mahoney J et al. (2009) FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis. Cell Stem Cell 5, 540– 553. 19896444 PMC3285492
  60. [69]Renault VM, Rafalski VA, Morgan AA, Salih DA, Brett JO, Webb AE, Villeda SA, Thekkat PU, Guillerey C, Denko NC et al. (2009) FoxO3 regulates neural stem cell homeostasis. Cell Stem Cell 5, 527– 539. 19896443 PMC2775802
  61. [71]Audesse AJ, Dhakal S, Hassell LA, Gardell Z, Nemtsova Y & Webb AE (2019) FOXO3 directly regulates an autophagy network to functionally regulate proteostasis in adult neural stem cells. PLoS Genet 15, e1008097. 30973875 PMC6478346
  62. [75]Moore DL, Pilz GA, Araúzo‐Bravo MJ, Barral Y & Jessberger S (2015) A mechanism for the segregation of age in mammalian neural stem cells. Science 349, 1334– 1338. 26383951
  63. [76]Loeffler D, Wehling A, Schneiter F, Zhang Y, Muller‐Botticher N, Hoppe PS, Hilsenbeck O, Kokkaliaris KD, Endele M & Schroeder T (2019) Asymmetric lysosome inheritance predicts activation of haematopoietic stem cells. Nature 573, 426– 429. 31485073
  64. [79]Filippi MD & Ghaffari S (2019) Mitochondria in the maintenance of hematopoietic stem cells: new perspectives and opportunities. Blood 133, 1943– 1952. 30808633 PMC6497515
  65. [80]Liang R, Arif T, Kalmykova S, Kasianov A, Lin M, Menon V, Qiu J, Bernitz JM, Moore K, Lin F et al. (2020) Restraining lysosomal activity preserves hematopoietic stem cell quiescence and potency. Cell Stem Cell 26, 359– 376.e7. 32109377 PMC8075247
  66. [81]Luis TC, Lawson H & Kranc KR (2020) Divide and rule: mitochondrial fission regulates quiescence in hematopoietic stem cells. Cell Stem Cell 26, 299– 301. 32142657
  67. [82]Beckervordersandforth R, Ebert B, Schaffner I, Moss J, Fiebig C, Shin J, Moore DL, Ghosh L, Trinchero MF, Stockburger C et al. (2017) Role of mitochondrial metabolism in the control of early lineage progression and aging phenotypes in adult hippocampal neurogenesis. Neuron 93, 560– 573.e6. 28111078 PMC5300896
  68. [83]Fujimaki K, Li R, Chen H, Della Croce K, Zhang HH, Xing J, Bai F & Yao G (2019) Graded regulation of cellular quiescence depth between proliferation and senescence by a lysosomal dimmer switch. Proc Natl Acad Sci USA 116, 22624– 22634. 31636214 PMC6842626
  69. [84]Gerisch B, Tharyan RG, Mak J, Denzel SI, Popkes‐van Oepen T, Henn N & Antebi A (2020) HLH‐30/TFEB is a master regulator of reproductive quiescence. Dev Cell 53, 316– 329.e5. 32302543
  70. [85]Ishii S, Matsuura A & Itakura E (2019) Identification of a factor controlling lysosomal homeostasis using a novel lysosomal trafficking probe. Sci Rep 9, 11635. 31406169 PMC6690932
  71. [86]Ba Q, Raghavan G, Kiselyov K & Yang G (2018) Whole‐cell scale dynamic organization of lysosomes revealed by spatial statistical analysis. Cell Rep 23, 3591– 3606. 29925001 PMC6086371
  72. [88]Mansueto G, Armani A, Viscomi C, D'Orsi L, De Cegli R, Polishchuk EV, Lamperti C, Di Meo I, Romanello V, Marchet S et al. (2017) Transcription factor EB controls metabolic flexibility during exercise. Cell Metab 25, 182– 196. 28011087 PMC5241227
  73. [89]Trivedi PC, Bartlett JJ, Mercer A, Slade L, Surette M, Ballabio A, Flibotte S, Hussein B, Rodrigues B, Kienesberger PC et al. (2020) Loss of function of transcription factor EB remodels lipid metabolism and cell death pathways in the cardiomyocyte. Biochim Biophys Acta Mol Basis Dis 1866, 165832. 32437957
  74. [90]Knobloch M (2017) The role of lipid metabolism for neural stem cell regulation. Brain Plast 3, 61– 71. 29765860 PMC5928532

Cited by

Sorted by citations

Authors
Kobayashi, T., & Kageyama, R.
Affiliations
Kyoto University (JP)
Corresponding author
  • Kobayashi, Taeko
  • Kageyama, Ryoichiro
ORCID
Venue
The FEBS Journal
Publisher
Wiley
Published
2020-09-15
Volume
288
Issue
10
Pages
3082-3093
ISSN
  • 1742-464X (ISSN-L)
  • 1742-4658
DOI
10.1111/febs.15555
PMC
PMC8246936
OpenAlex
W3086526810
Cited by
28
References
15
Citations by year
2026: 3 · 2025: 2 · 2024: 10 · 2023: 2 · 2022: 7 · 2021: 4
FWCI
0.51
Type
journal article
Language
en
Open access
Licence
Locations
  • FEBS Journal (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • Ministry of Education, Culture, Sports, Science and Technology (16H06480)
  • Japan Agency for Medical Research and Development (JP18gm1110002h0002)
  • Japan Society for the Promotion of Science (JSPS 20H03260)
  • Kyoto University
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
neural stem cells, quiescence, lysosomes, proteostasis, BMP signaling, Notch signaling, stem cell niche, cell cycle arrest, protein degradation, self-renewal
MeSH terms
Proteostasis, Cell Cycle, Cell Differentiation, Gene Expression Regulation, Humans, Lysosomes, Neuroglia, Neurons, Signal Transduction, Bone Morphogenetic Proteins, Cell Proliferation, Receptors, Notch, Adult Stem Cells, Stem Cell Niche, Neurogenesis, Neural Stem Cells

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review