Affinage

GSX2

GS homeobox 2 · UniProt Q9BZM3

Length
304 aa
Mass
32.0 kDa
Annotated
2026-04-28
49 papers in source corpus 23 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GSX2 is a homeodomain transcription factor that patterns the ventral telencephalon and specifies neuronal subtype identity during development. Operating downstream of Sonic Hedgehog signaling, GSX2 cross-represses the dorsal determinant PAX6 to maintain lateral ganglionic eminence (LGE) progenitor identity, promotes retinoid synthesis via Raldh3 for striatal neuron differentiation, and suppresses oligodendrocyte precursor specification from LGE progenitors (PMID:11003836, PMID:15269172, PMID:23637331). GSX2 gains transcriptional specificity through cooperative homodimerization on DNA sites spaced 7 bp apart—monomer binding represses while dimer binding activates transcription—and physically interacts with the bHLH domain of ASCL1 to inhibit its DNA binding and restrain neurogenesis in progenitors (PMID:33334823, PMID:38874471, PMID:32122989). Recessive loss-of-function variants in GSX2 cause human basal ganglia agenesis, and a knock-in disease-associated homeodomain missense mutation demonstrates that graded reductions in DNA-binding activity differentially affect distinct neuronal subtypes (PMID:31412107, PMID:39882631).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1995 Medium

    Establishing GSX2 as a sequence-specific transcription factor answered the fundamental question of whether this homeodomain protein has defined DNA-binding specificity, providing the basis for all subsequent target gene analyses.

    Evidence SELEX (random oligonucleotide selection/PCR) identified the CNAATTAG consensus binding site from cloned cDNA

    PMID:7619729

    Open questions at the time
    • Single in vitro method without in vivo validation of binding sites
    • No information on target genes or transcriptional output
    • Binding specificity not compared with paralog GSX1
  2. 1997 High

    The first knockout demonstrated that GSX2 is essential for LGE patterning and hindbrain development, converting it from a cloned gene to a required developmental regulator.

    Evidence Targeted gene knockout in mice with histological and molecular marker analysis

    PMID:9398437

    Open questions at the time
    • Mechanism of action (activator vs. repressor) unknown
    • Direct target genes not identified
    • Functional relationship with other ventral transcription factors undefined
  3. 2000 High

    Cross-repression between GSX2 and PAX6 was established as the mechanism positioning the pallial–subpallial boundary, and GSX2 was placed downstream of Shh signaling, resolving how ventral identity is established and maintained.

    Evidence Single and double loss-of-function mouse mutants with genetic epistasis; Shh pathway perturbation with in situ hybridization

    PMID:11003836 PMID:11060228 PMID:11124115

    Open questions at the time
    • Whether GSX2 directly represses Pax6 transcription or acts indirectly not determined
    • Mechanism by which Shh induces Gsx2 expression unknown
  4. 2001 High

    Discovery of functional redundancy between GSX1 and GSX2 in LGE patterning revealed that GSX1 partially compensates for GSX2 loss, explaining why single mutants retain some ventral identity.

    Evidence Gsx1/Gsx2 double knockout mice with quantitative marker analysis

    PMID:11731457

    Open questions at the time
    • Molecular basis of functional overlap versus divergence between paralogs not defined
    • Whether the two paralogs share identical target genes unknown
  5. 2003 High

    GSX2 was shown to cooperate with NKX2.1 in early ventral patterning but antagonize NKX2.1-dependent oligodendrocyte specification later, revealing context-dependent interactions between ventral homeodomain factors.

    Evidence Double mutant mouse analysis with gain-of-function and loss-of-function approaches

    PMID:12930780

    Open questions at the time
    • Whether antagonism is direct transcriptional repression or indirect circuit-level effect not resolved
    • Temporal switch mechanism unknown
  6. 2004 High

    Placing GSX2 upstream of retinoid synthesis (via Raldh3) for striatal neuron differentiation identified the first signaling pathway through which GSX2 executes neuronal subtype specification.

    Evidence Gsx2 knockout mice showing reduced retinoid production; exogenous retinoic acid rescued DARPP-32 neuron differentiation

    PMID:15269172

    Open questions at the time
    • Whether Raldh3 is a direct transcriptional target of GSX2 not demonstrated
    • Other downstream effectors of GSX2 in striatal differentiation not identified
  7. 2009 High

    Temporal dissection revealed that GSX2 specifies striatal projection neurons at early stages and olfactory bulb interneurons at later stages, establishing that the same transcription factor produces distinct neuronal subtypes depending on developmental timing.

    Evidence Temporally regulated transgenic gain-of-function and conditional loss-of-function in mice

    PMID:19709628

    Open questions at the time
    • Molecular basis for temporal switch in subtype specification unknown
    • Whether cofactor availability changes over time not addressed
  8. 2013 High

    Multiple studies converged to show that GSX2 suppresses the neurogenesis-to-oligodendrogenesis switch, maintains adult SVZ neural stem cell activation, and interacts with Dlx factors in a gene-specific epistatic hierarchy, broadening GSX2's roles beyond embryonic patterning.

    Evidence Conditional gain- and loss-of-function mouse models for OPC specification; conditional adult KO with BrdU labeling; compound Dlx1/2;Gsx2 triple KO analysis

    PMID:23042297 PMID:23637331 PMID:23723414

    Open questions at the time
    • Direct versus indirect mechanisms of OPC suppression not distinguished
    • Whether adult SVZ function uses the same target genes as embryonic LGE not known
  9. 2018 High

    Identification of DMRT3, DMRT5, and EMX2 as cooperative repressors of a Gsx2 enhancer explained how GSX2 expression is restricted at the pallial–subpallial boundary, closing the loop on upstream regulation.

    Evidence Double knockout mice plus ChIP showing direct binding of DMRT3, DMRT5, and EMX2 to a Gsx2 ventral telencephalon enhancer

    PMID:30143575

    Open questions at the time
    • Full cis-regulatory architecture of the Gsx2 locus not mapped
    • Whether additional repressors contribute not assessed
  10. 2019 Medium

    Human genetic evidence linked recessive GSX2 loss-of-function to basal ganglia agenesis, validating the mouse patterning role in human neurodevelopment and identifying a disease-associated homeodomain mutation (Q251R) that impairs DNA binding and nuclear localization.

    Evidence Whole-exome sequencing of affected families; molecular dynamics simulation; transfection assays; patient fibroblast transcriptomics

    PMID:31412107

    Open questions at the time
    • Structural impact of Q251R assessed by modeling rather than crystallography
    • Limited number of families studied
    • Functional validation performed in fibroblasts rather than neural progenitors
  11. 2020 High

    The cooperative homodimerization mechanism was elucidated: GSX2 monomers repress while dimers on spaced sites activate transcription, and GSX2 physically sequesters ASCL1 away from DNA to restrain neurogenesis, providing the first unified model of how GSX2 acts as both repressor and activator.

    Evidence ChIP-seq in mouse ventral telencephalon, luciferase reporters in mouse and Drosophila; co-immunoprecipitation, proximity ligation assay, and DNA-binding interference assays for ASCL1 interaction

    PMID:32122989 PMID:33334823

    Open questions at the time
    • Full repertoire of direct activating versus repressing targets genome-wide not catalogued
    • Whether ASCL1 interaction is modulated by developmental stage not tested
  12. 2024 High

    Crystal structure of the GSX2 homeodomain–DNA complex resolved the structural basis of cooperative dimerization: GSX2 is a monomer in solution, requires DNA for dimer formation, induces a 20° DNA bend, and uses a specific protein–protein interface for cooperativity.

    Evidence X-ray crystallography, ITC, SPR, and mutagenesis of the cooperativity interface

    PMID:38874471

    Open questions at the time
    • Full-length protein structure not determined
    • Structural basis of ASCL1 interaction not resolved
    • How the 20° bend contributes to transcriptional output not established
  13. 2025 High

    A knock-in mouse carrying the disease-associated Q252R mutation demonstrated that graded reductions in DNA-binding activity differentially affect neuronal subtypes, establishing a threshold model for GSX2 function and showing the mutation is hypomorphic rather than null.

    Evidence Knock-in mouse model with biochemical DNA-binding assays and histological phenotyping

    PMID:39882631

    Open questions at the time
    • Which specific target gene thresholds underlie differential subtype vulnerability unknown
    • Whether cooperative dimerization is selectively affected by Q252R not tested
  14. 2026 High

    Genome-wide binding and transcriptomic profiling in human LGE-like progenitors established that GSX2 functions primarily as a transcriptional repressor, binds both open and closed chromatin, and alters chromatin accessibility largely through indirect mechanisms, extending the monomer-repressor model to a human system.

    Evidence Dox-inducible hESC differentiation with integrated RNA-seq, ATAC-seq, and ChIP-seq

    PMID:41512913

    Open questions at the time
    • Whether dimer-dependent activation seen in mouse also operates in human progenitors not distinguished
    • Indirect chromatin remodeling mechanism not identified
    • Limited to one hESC line

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the full direct target gene network distinguishing monomer-repressed from dimer-activated genes in vivo, the structural basis of the GSX2–ASCL1 interaction, how temporal changes in cofactor availability switch GSX2 output from striatal to olfactory bulb fates, and whether GSX2 silencing contributes to human glioma pathogenesis.
  • No genome-wide distinction of direct monomer vs. dimer targets in vivo
  • GSX2–ASCL1 interaction interface not structurally resolved
  • Temporal cofactor switching mechanism unknown
  • Role in gliomagenesis based on single preprint

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0003677 DNA binding 5 GO:0098772 molecular function regulator activity 1
Localization
GO:0005634 nucleus 2
Pathway
R-HSA-1266738 Developmental Biology 6 R-HSA-112316 Neuronal System 4
Partners
ASCL1DLX1DLX2DMRT5EMX2GSX1NKX2-1PAX6

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 Gsh-2 encodes a homeodomain protein with an Antennapedia-type homeodomain; a random oligonucleotide selection and PCR amplification procedure defined its target DNA binding sequence as CNAATTAG, establishing it as a sequence-specific transcription factor. cDNA cloning, SELEX (random oligonucleotide selection + PCR) Mechanisms of development Medium 7619729
1997 Loss of Gsh-2 in mouse knockouts results in a reduced lateral ganglionic eminence (LGE), absence of Dlx2 expression in the LGE, and severe hindbrain defects including absence of the area postrema and malformation of the nucleus tractus solitarius, demonstrating Gsh-2 is required for LGE patterning and hindbrain development. Targeted gene knockout in mice, in situ hybridization, immunohistochemistry Developmental biology High 9398437
2000 Gsh2 is required to maintain the molecular identity of early striatal progenitors in the LGE; in its absence, ventral markers Mash1 and Dlx are lost and dorsal markers Pax6, Ngn1, and Ngn2 are ectopically expressed. Conversely, Pax6 and Gsh2 mutually repress each other, as shown by double-mutant rescue of both cortical and striatal progenitor specification defects. Single and double loss-of-function mouse mutants, in situ hybridization, genetic epistasis Development (Cambridge, England) High 11003836
2000 Gsh2 is a downstream transcriptional target of sonic hedgehog (Shh) signaling in the ventral telencephalon, and its loss causes early expansion of dorsal telencephalic markers across the cortical-striatal boundary with subsequent delay in GABAergic interneuron appearance in the olfactory bulb. Gsh2 knockout mouse analysis, in situ hybridization, Shh pathway perturbation Development (Cambridge, England) High 11060228
2001 Gsh2 and Pax6 have complementary roles at the pallial/subpallial boundary: in Gsh2 mutants the dorsal LGE is respecified into a ventral pallium-like structure, while in Pax6 mutants the ventral pallium is respecified into a dLGE-like structure, establishing that these two transcription factors cross-repress each other to define regional identity. Single and double loss-of-function mouse mutants, in situ hybridization Development (Cambridge, England) High 11124115
2001 Gsh1 functionally compensates for Gsh2 loss in the LGE: Gsh1 expression expands in Gsh2−/− LGE, and Gsh1/Gsh2 double mutants show more severe disruption of LGE molecular identity and progenitor pool size than Gsh2 single mutants, demonstrating partial functional redundancy. Single and double knockout mouse mutants, in situ hybridization, cell counting Development (Cambridge, England) High 11731457
2003 Gsh2 and Nkx2.1 act cooperatively (not via cross-repression) to pattern the ventral telencephalon; however, Gsh2 expression in the MGE after E10.5 negatively regulates Nkx2.1-dependent oligodendrocyte specification, revealing both integrative and antagonistic interactions between these homeodomain factors. Double mutant mouse analysis, gain-of-function, loss-of-function, in situ hybridization Development (Cambridge, England) High 12930780
2004 Gsh2 is required for expression of the retinoic acid synthesis enzyme Raldh3 (Aldh1a3) in the LGE; Gsh2 mutants show markedly reduced retinoid production, and supplementation with exogenous retinoic acid during striatal neurogenesis rescues DARPP-32 neuron differentiation in Gsh2 mutants, placing Gsh2 upstream of retinoid signaling for striatal differentiation. Gsh2 knockout mice, in situ hybridization, retinoid reporter cell assay, retinoic acid supplementation rescue experiment Development (Cambridge, England) High 15269172
2005 In the dorsal spinal cord, Gsh2 specifies dI3 interneuron fate by repressing Ngn1 and promoting Mash1 expression in dI3 progenitors; overexpression of Gsh2 together with Mash1 leads to ectopic dI3 neuron production and Ngn1 repression. Gsh2 knockout mice, overexpression, in situ hybridization, genetic epistasis with Mash1 mutants Development (Cambridge, England) High 15930101
2009 Gsx2 specifies striatal projection neuron identity when active at early stages of telencephalic neurogenesis, and olfactory bulb interneuron identity when activated at later stages; conditional temporal inactivation shows that loss of Gsx2 at early stages spares striatal development but impairs olfactory bulb interneuron production. Temporally regulated transgenic gain-of-function and conditional loss-of-function in mice, neuronal marker analysis Neuron High 19709628
2010 In Xenopus, Gsh2 mediates transcriptional repression of Dbx1 as a direct target, and cross-repressive interactions between Gsx, Dbx, and Nkx factors pattern the medial neural plate; however, the unidirectional Drosophila Msx/Nkx/Gsx interaction system is not conserved in Xenopus. Gain- and loss-of-function in Xenopus embryos, reporter assays, in situ hybridization Development (Cambridge, England) Medium 20610487
2012 Helios transcription factor expression in striatal matrix neurons requires Gsx2 and Dlx1/2 but is independent of Ascl1, placing Gsx2 upstream of Helios in the LGE transcriptional cascade for striatal matrix neuron specification. Gsx2, Dlx1/2, and Ascl1 null mutant mouse analysis, immunofluorescence, in situ hybridization Stem cells and development Medium 22142223
2013 Gsx2 suppresses oligodendrocyte precursor cell (OPC) specification from dLGE progenitors during neurogenic stages; loss of Gsx2 increases OPCs in the cortex (derived from dLGE via Ascl1-dependent mechanism), while gain-of-function at late stages decreases cortical OPCs, demonstrating Gsx2 controls the neurogenesis-to-oligodendrogenesis switch. Conditional gain- and loss-of-function mouse models, Olig2-Cre conditional KO, cell counting, marker analysis Development (Cambridge, England) High 23637331
2013 In the adult mouse subventricular zone, Gsx2 is expressed in a regionally restricted subset of neural stem cells (NSCs) and promotes their activation and lineage progression to produce selective olfactory bulb neuron subtypes; Gsx2 is also ectopically induced after brain injury and is required for injury-induced neurogenesis in the SVZ. Conditional Gsx2 loss-of-function in adult mice, BrdU/EdU labeling, immunofluorescence, fate mapping Genes & development High 23723414
2013 Loss of Gsx2 in Dlx1/2 mutant background rescues increased Ascl1, Hes5, and Olig2 expression, while Dlx1/2;Gsx2 compound mutants exacerbate LGE patterning defects and lose GAD1 expression; Gsx1 removal from Dlx1/2 mutants partially rescues MGE properties and cortical interneuron migration, revealing distinct functional interactions of Gsx2 versus Gsx1 with Dlx factors. Compound loss-of-function mouse mutants (triple KO combinations), in situ hybridization, immunofluorescence The Journal of comparative neurology High 23042297
2018 DMRT3, DMRT5, and EMX2 cooperatively repress Gsx2 at the pallial-subpallial boundary to maintain cortical identity; all three transcription factors bind a ventral telencephalon-specific enhancer in the Gsx2 locus. Double knockout mice, ectopic Dmrt5 expression, ChIP/genomic binding assays for DMRT3, DMRT5, and EMX2 on Gsx2 enhancer The Journal of neuroscience High 30143575
2019 Recessive loss-of-function variants in GSX2 cause human basal ganglia agenesis; a homeodomain missense variant (Q251R) reduces protein expression, impairs DNA binding (shown by molecular dynamics), reduces nuclear localization in transfected cells, and alters transcriptional self-regulation as well as ASCL1 and PAX6 expression in patient fibroblasts. Whole-exome sequencing, molecular dynamics simulation, transfection/nuclear localization assay, patient fibroblast transcriptomics Brain : a journal of neurology Medium 31412107
2020 Gsx2 gains DNA-binding specificity by forming cooperative homodimers on precisely spaced and oriented DNA sites (7 bp apart); monomer Gsx2 binding represses transcription while homodimer binding stimulates gene expression, as demonstrated by high-resolution genomic binding assays (ChIP) in the developing mouse ventral telencephalon and reporter assays in both mouse and Drosophila. ChIP-seq (high-resolution genomic binding), luciferase reporter assays, Drosophila enhancer analysis Genes & development High 33334823
2020 Gsx2 physically interacts with the bHLH domain of Ascl1 in LGE ventricular zone progenitors; this interaction interferes with Ascl1 DNA binding in a dose-dependent manner and inhibits Ascl1-driven neurogenesis, thereby balancing progenitor maintenance versus differentiation. Luciferase reporter assays, co-immunoprecipitation, DNA-binding assays, proximity ligation assay in tissue sections Development (Cambridge, England) High 32122989
2024 Gsx2 is a monomer in solution and requires DNA for cooperative homodimer complex formation; crystal structure of the Gsx2 homeodomain-DNA monomer complex reveals that Gsx2 induces a 20° bend in DNA; a specific protein-protein interface in the homeodomain is required for cooperative homodimer DNA binding; flexible spacer DNA sequences enhance cooperativity. X-ray crystallography, biophysical binding assays (ITC, SPR), biochemical assays, mutagenesis of protein-protein interface Nucleic acids research High 38874471
2025 The Gsx2Q252R homeodomain missense variant selectively alters DNA binding; mice carrying this allele exhibit basal ganglia dysgenesis but survive (unlike null mice), with relative sparing of glutamatergic nTS neurons and catecholaminergic groups, demonstrating that distinct thresholds of DNA-binding activity specify different neuronal subtypes. Knock-in mouse model, biochemical DNA-binding assays, histological and immunofluorescence analysis of brain phenotypes Disease models & mechanisms High 39882631
2025 Mutant IDH causes promoter hypermethylation and silencing of Gsx2 in neural progenitor cells, resulting in lineage switching from interneurons to oligodendrocyte precursor cells and promoting gliomagenesis; Gsx2 ablation alone recapitulates this NPC fate reprogramming. Genetically engineered mouse model, single-cell RNA-seq, epigenomic profiling, Gsx2 conditional knockout bioRxivpreprint Medium 40832272
2026 In human LGE-like progenitors derived from hESCs, GSX2 binds both high- and low-accessibility chromatin using varying binding site preferences, alters chromatin accessibility largely through indirect mechanisms, and functions primarily as a transcriptional repressor of key conserved target genes affecting neuronal progenitor maturation and regional specification. Dox-inducible hESC system, RNA-seq, ATAC-seq, ChIP-seq (genomic binding studies) Developmental biology High 41512913

Source papers

Stage 0 corpus · 49 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 Gsh2 and Pax6 play complementary roles in dorsoventral patterning of the mammalian telencephalon. Development (Cambridge, England) 389 11124115
2000 Genetic control of dorsal-ventral identity in the telencephalon: opposing roles for Pax6 and Gsh2. Development (Cambridge, England) 336 11003836
2000 The Gsh2 homeodomain gene controls multiple aspects of telencephalic development. Development (Cambridge, England) 195 11060228
2005 Differential targeting of GSH1 and GSH2 is achieved by multiple transcription initiation: implications for the compartmentation of glutathione biosynthesis in the Brassicaceae. The Plant journal : for cell and molecular biology 176 15610346
2001 A role for Gsh1 in the developing striatum and olfactory bulb of Gsh2 mutant mice. Development (Cambridge, England) 141 11731457
2009 Distinct temporal requirements for the homeobox gene Gsx2 in specifying striatal and olfactory bulb neuronal fates. Neuron 112 19709628
2003 Combinatorial function of the homeodomain proteins Nkx2.1 and Gsh2 in ventral telencephalic patterning. Development (Cambridge, England) 100 12930780
1997 Altered forebrain and hindbrain development in mice mutant for the Gsh-2 homeobox gene. Developmental biology 90 9398437
1995 Gsh-2, a murine homeobox gene expressed in the developing brain. Mechanisms of development 77 7619729
2013 Gsx2 controls region-specific activation of neural stem cells and injury-induced neurogenesis in the adult subventricular zone. Genes & development 76 23723414
2013 Loss of Gsx1 and Gsx2 function rescues distinct phenotypes in Dlx1/2 mutants. The Journal of comparative neurology 65 23042297
2008 Differential regulation of telencephalic pallial-subpallial boundary patterning by Pax6 and Gsh2. Cerebral cortex (New York, N.Y. : 1991) 60 18701439
2013 The homeobox gene Gsx2 controls the timing of oligodendroglial fate specification in mouse lateral ganglionic eminence progenitors. Development (Cambridge, England) 49 23637331
1998 Molecular identification of glutathione synthetase (GSH2) gene from Saccharomyces cerevisiae. Biochimica et biophysica acta 43 9512666
2005 Gsh2 is required for the repression of Ngn1 and specification of dorsal interneuron fate in the spinal cord. Development (Cambridge, England) 42 15930101
2004 The homeobox gene Gsh2 is required for retinoid production in the embryonic mouse telencephalon. Development (Cambridge, England) 38 15269172
2017 Differentiation of human telencephalic progenitor cells into MSNs by inducible expression of Gsx2 and Ebf1. Proceedings of the National Academy of Sciences of the United States of America 32 28137879
1996 Cloning of the cDNA and genomic clones for glutathione synthetase from Arabidopsis thaliana and complementation of a gsh2 mutant in fission yeast. Plant molecular biology 32 8914526
2018 DMRT5, DMRT3, and EMX2 Cooperatively Repress Gsx2 at the Pallium-Subpallium Boundary to Maintain Cortical Identity in Dorsal Telencephalic Progenitors. The Journal of neuroscience : the official journal of the Society for Neuroscience 30 30143575
1996 Cloning of Arabidopsis thaliana glutathione synthetase (GSH2) by functional complementation of a yeast gsh2 mutant. European journal of biochemistry 28 8612643
2012 Helios transcription factor expression depends on Gsx2 and Dlx1&2 function in developing striatal matrix neurons. Stem cells and development 26 22142223
2020 Conserved Gsx2/Ind homeodomain monomer versus homodimer DNA binding defines regulatory outcomes in flies and mice. Genes & development 25 33334823
2010 Conserved and novel roles for the Gsh2 transcription factor in primary neurogenesis. Development (Cambridge, England) 23 20610487
2020 Physical interactions between Gsx2 and Ascl1 balance progenitor expansion versus neurogenesis in the mouse lateral ganglionic eminence. Development (Cambridge, England) 22 32122989
2020 Transcription factor Hap5 induces gsh2 expression to enhance 2-phenylethanol tolerance and production in an industrial yeast Candida glycerinogenes. Applied microbiology and biotechnology 22 32162090
2017 Septal contributions to olfactory bulb interneuron diversity in the embryonic mouse telencephalon: role of the homeobox gene Gsx2. Neural development 21 28814342
2009 Cloning and expression analysis of the anterior parahox genes, Gsh1 and Gsh2 from Xenopus tropicalis. Developmental dynamics : an official publication of the American Association of Anatomists 20 19097192
2012 The homeobox gene Gsx2 regulates the self-renewal and differentiation of neural stem cells and the cell fate of postnatal progenitors. PloS one 19 22242181
2002 Expression of Ngn1, Ngn2, Cash1, Gsh2 and Sfrp1 in the developing chick telencephalon. Mechanisms of development 18 11744393
2004 Striatal neuron differentiation from neurosphere-expanded progenitors depends on Gsh2 expression. The Journal of neuroscience : the official journal of the Society for Neuroscience 13 15295031
2019 Agenesis of the putamen and globus pallidus caused by recessive mutations in the homeobox gene GSX2. Brain : a journal of neurology 12 31412107
2016 Characterization of a new Gsx2-cre line in the developing mouse telencephalon. Genesis (New York, N.Y. : 2000) 12 27618396
2020 Gsx2 is required for specification of neurons in the inferior olivary nuclei from Ptf1a-expressing neural progenitors in zebrafish. Development (Cambridge, England) 11 32928905
2002 GSH2, a gene encoding gamma-glutamylcysteine synthetase in the methylotrophic yeast Hansenula polymorpha. FEMS yeast research 11 12702282
2021 Transcription Factor VAX1 Regulates the Regional Specification of the Subpallium Through Repressing Gsx2. Molecular neurobiology 9 33821423
2017 Effects of GSH1 and GSH2 Gene Mutation on Glutathione Synthetases Activity of Saccharomyces cerevisiae. The protein journal 7 28669025
2024 Cooperative Gsx2-DNA binding requires DNA bending and a novel Gsx2 homeodomain interface. Nucleic acids research 5 38874471
2015 GSH2 promoter methylation in pancreatic cancer analyzed by quantitative methylation-specific polymerase chain reaction. Oncology letters 5 26171036
2012 Preparation of a γ-glutamylcysteine-enriched yeast extract from a newly developed GSH2-deficient strain. Journal of bioscience and bioengineering 3 22986308
2022 Gsx2, but not Gsx1, is necessary for early forebrain patterning and long-term survival in zebrafish. Developmental dynamics : an official publication of the American Association of Anatomists 2 36184733
2002 [Cloning of the GSH1 and GSH2 genes complementing the defective biosynthesis of glutathione in the methylotrophic yeast Hansenula polymorpha]. Mikrobiologiia 2 12526206
2025 Modelling a pathological GSX2 variant that selectively alters DNA binding reveals hypomorphic mouse brain defects. Disease models & mechanisms 1 39882631
2025 Mutant IDH silences GSX2 to reprogram neural progenitor cell fate and promote gliomagenesis. bioRxiv : the preprint server for biology 1 40832272
2023 Cooperative Gsx2-DNA Binding Requires DNA Bending and a Novel Gsx2 Homeodomain Interface. bioRxiv : the preprint server for biology 1 38106145
2014 [Transcriptional regulation of the Hansenula polymorpha GSH2 gene in response to cadmium ion treatment]. Ukrainian biochemical journal 1 24834720
2026 Gsx2 regulates oligodendrocyte precursor formation in the zebrafish spinal cord. Developmental biology 0 41491310
2026 An inducible system to study the regulatory functions of GSX2 in human lateral ganglionic eminence-like progenitors. Developmental biology 0 41512913
2025 Gsx2 Regulates Oligodendrocyte Precursor Formation in the Zebrafish Spinal Cord. bioRxiv : the preprint server for biology 0 41279990
2020 A CRISPR-strategy for the generation of a detectable fluorescent hESC reporter line (WAe009-A-37) for the subpallial determinant GSX2. Stem cell research 0 33039807