Olig gene function in CNS development and disease
Abstract
Olig1 and Olig2 encode basic helix‐loop‐helix (bHLH) transcription factors that are expressed in both the developing and mature vertebrate central nervous system. While numerous studies have established critical functions for Olig genes during the formation of motor neurons and oligodendrocytes of the ventral neural tube, their roles at later stages of development and in adulthood have remained relatively obscure. Recent studies, however, reveal that in the fetal dorsal spinal cord and neural progenitor cells of the adult brain, Olig expression continues to mark, and may regulate, the formation of oligodendroglia. Studies of Olig expression in human brain tumors and repair of demyelinating lesions suggest the possibility of additional functions in a variety of neurological diseases. © 2005 Wiley‐Liss, Inc.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
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?
OLIG2 is a chromosome 21-encoded gene that is a master regulator for oligodendrocyte development.
“Much of the work in DS has focused on OLIG2, a chromosome 21-encoded gene that is a master regulator for oligodendrocyte development92,93,108.”
From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [92]
Cites
Neuronal specification in the spinal cord: inductive signals and transcriptional codes
Jessell, T. M. (2000) · Nature Reviews Genetics · doi:10.1038/35049541 · Cited by 2,089 · see citing works
Compston, A., & Coles, A. (2002) · The Lancet · doi:10.1016/s0140-6736(02)08220-x · Cited by 1,743 · see citing works
The bHLH Transcription Factors OLIG2 and OLIG1 Couple Neuronal and Glial Subtype Specification
Zhou, Q., & Anderson, D. J. (2002) · Cell · doi:10.1016/s0092-8674(02)00677-3 · Cited by 1,059 · see citing works
Dawson, M. (2003) · Molecular and Cellular Neuroscience · doi:10.1016/s1044-7431(03)00210-0 · Cited by 927 · see citing works
bHLH Transcription Factor Olig1 Is Required to Repair Demyelinated Lesions in the CNS
Arnett, H. A., Fancy, S. P. J., Alberta, J. A., Zhao, C., Plant, S. R., Kaing, S., Raine, C. S., Rowitch, D. H., Franklin, R. J. M., & Stiles, C. D. (2004) · Science · doi:10.1126/science.1103709 · Cited by 416 · see citing works
Self-citationMimault, C., Giraud, G., Courtois, V., Cailloux, F., Boire, J. Y., Dastugue, B., & Boespflug-Tanguy, O. (1999) · The American Journal of Human Genetics · doi:10.1086/302483 · Cited by 133 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Timing Is Everything: Making Neurons versus Glia in the Developing Cortex
Miller, F. D., & Gauthier, A. S. (2007) · Neuron · doi:10.1016/j.neuron.2007.04.019 · Cited by 588 · see citing works
Dimou, L., Simon, C., Kirchhoff, F., Takebayashi, H., & Götz, M. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.2831-08.2008 · Cited by 551 · see citing works
Identification of diverse astrocyte populations and their malignant analogs
John Lin, C.-C., Yu, K., Hatcher, A., Huang, T.-W., Lee, H. K., Carlson, J., Weston, M. C., Chen, F., Zhang, Y., Zhu, W., et al. (2017) · Nature Neuroscience · doi:10.1038/nn.4493 · Cited by 525 · see citing works
Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned
Gudi, V., Gingele, S., Skripuletz, T., & Stangel, M. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00073 · Cited by 375 · see citing works
“Keywords: cuprizone mouse model, remyelination, demyelination, growth factors, microglia, astrocytes”
BackgroundOxidative stress disrupts oligodendrocyte maturation
French, H. M., Reid, M., Mamontov, P., Simmons, R. A., & Grinspan, J. B. (2009) · Journal of Neuroscience Research · doi:10.1002/jnr.22139 · Cited by 246 · see citing works
De Biase, L. M., Kang, S. H., Baxi, E. G., Fukaya, M., Pucak, M. L., Mishina, M., Calabresi, P. A., & Bergles, D. E. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.2455-11.2011 · Cited by 161 · see citing works
El-Etr, M., Rame, M., Boucher, C., Ghoumari, A. M., Kumar, N., Liere, P., Pianos, A., Schumacher, M., & Sitruk-Ware, R. (2015) · Glia · doi:10.1002/glia.22736 · Cited by 116 · see citing works
Pentón-Rol, G., Marín-Prida, J., & McCarty, M. F. (2021) · Current Neuropharmacology · doi:10.2174/1570159x19666210408123807 · Cited by 73 · see citing works
Pentón-Rol, G., Marín-Prida, J., & Falcón-Cama, V. (2018) · Behavioral Sciences · doi:10.3390/bs8010015 · Cited by 50 · see citing works
Fang, F., Zhang, H., Zhang, Y., Xu, H., Huang, Q., Adilijiang, A., Wang, J., Zhang, Z., Zhang, D., Tan, Q., et al. (2013) · Life Sciences · doi:10.1016/j.lfs.2013.08.004 · Cited by 36 · see citing works
Consequences of trisomy 21 for brain development in Down syndrome
Russo, M. L., Sousa, A. M. M., & Bhattacharyya, A. (2024) · Nature Reviews Neuroscience · doi:10.1038/s41583-024-00866-2 · Cited by 28 · see citing works
“…progenitors expressing the marker OLIG2, a HSA21-encoded transcription factor important for regulating ventral fate and oligodendrogliogenesis 92,93 , and has assessed their fate in organoids and chimaeras 91 , whereas other studies have used two-dimensional cultures to drive the…”
- Authors
- Ligon, K. L., Fancy, S. P. J., Franklin, R. J. M., & Rowitch, D. H.
- Affiliations
- Brigham and Women's Hospital (US)
- University of Cambridge (GB)
- Harvard University (US)
- Corresponding author
- Rowitch, David H.
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2006-05
- Volume
- 54
- Issue
- 1
- Pages
- 1-10
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W1998444616
- Cited by
- 223
- References
- 6
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 6 · 2023: 2 · 2022: 4 · 2021: 8 · 2020: 6 · 2019: 4 · 2018: 7 · 2017: 8 · 2016: 7 · 2015: 11 · 2014: 21 · 2013: 22 · 2012: 13
- FWCI
- 1.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- 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 › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- Olig1, Olig2, bHLH transcription factors, central nervous system development, motor neurons, oligodendrocyte differentiation, dorsal spinal cord, neural progenitor cells, oligodendroglia, brain tumors, demyelination, neurological disorders
- MeSH terms
- Animals, Brain Neoplasms, Cell Differentiation, Central Nervous System, Demyelinating Diseases, Humans, Nerve Tissue Proteins, Oligodendroglia, Stem Cells, Gene Expression Regulation, Developmental, Cell Lineage, Basic Helix-Loop-Helix Proteins
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
