Nurr1, an orphan nuclear receptor, is a transcriptional activator of endogenous tyrosine hydroxylase in neural progenitor cells derived from the adult brain.
Sakurada K, Ohshima-Sakurada M, Palmer TD, Gage FH
Nurr1 directly activates the tyrosine hydroxylase gene in neural progenitor cells, establishing a key step in dopaminergic neuron development. This activation occurs independently of other patterning signals and does not trigger cell differentiation or proliferation.
- Nurr1 binds to the tyrosine hydroxylase promoter to activate its transcription.
- This mechanism operates independently of retinoid X receptor signaling pathways.
- Nurr1 overexpression does not cause neural progenitor cells to differentiate or proliferate.
- The study uses adult rat hippocampal progenitor cells, not human tissue.
Organization of the human orphan nuclear receptor Nurr1 gene.
Torii T, Kawarai T, Nakamura S, Kawakami H
This study maps the structure and regulatory regions of the human NR4A2 gene, confirming its genetic organization is highly conserved between humans and mice. It identifies specific DNA sequences that control when and how much Nurr1 protein is produced in cells.
- The human NR4A2 gene spans approximately 8.3kb with eight exons and seven introns.
- Its genomic structure closely matches the mouse version, supporting animal model relevance.
- Three regulatory elements control gene expression in response to cellular signals.
- The findings provide a baseline for studying genetic variations linked to dopamine disorders.
Molecular cloning of the human Nurr1 gene: characterization of the human gene and cDNAs.
Ichinose H, Ohye T, Suzuki T, Sumi-Ichinose C, Nomura T, Hagino Y, Nagatsu T
Researchers identified the complete DNA sequence and structure of the human Nurr1 gene, confirming it consists of eight exons. They also discovered a new version of the Nurr1 protein produced by alternative splicing in the fetal brain.
- The study maps the full genetic structure of human Nurr1 for the first time.
- It identifies specific regulatory regions that control how the gene is turned on or off.
- A new protein variant resulting from RNA splicing exists in the developing human brain.
Activity-dependent Nurr1 and NGFI-B gene expression in adult mouse olfactory bulb.
Liu N, Baker H
This study shows that Nurr1 and NGFI-B genes are active in the adult mouse olfactory bulb and decrease when smell is blocked. It suggests these receptors help regulate dopamine-related functions in this specific brain region, distinct from their known role in midbrain development.
- Nurr1 and NGFI-B mRNAs exist in mouse olfactory bulb layers.
- Odor deprivation reduces levels of both receptors and tyrosine hydroxylase.
- Findings suggest a role for these genes in adult olfactory dopamine regulation.
- Study uses only adult mice, not human patients or clinical data.
An isoform of Nurr1 functions as a negative inhibitor of the NGFI-B family signaling.
Ohkura N, Hosono T, Maruyama K, Tsukada T, Yamaguchi K
Researchers identified a truncated version of the NR4A2 protein, called Nurr2, which acts as a brake on normal NR4A2 signaling. This isoform lacks the parts of the protein needed to activate genes but still binds to DNA to block other family members from working. The study confirms this mechanism occurs in human cells and tissues.
- Nurr2 is a truncated NR4A2 isoform found in mouse, rat, and human tissues.
- It lacks the ligand-binding and dimerization domains of full-length Nurr1.
- Nurr2 inhibits gene activation by other NGFI-B family members like Nurr1.
- The protein is highly expressed in the pituitary gland and cerebral cortex.
Prolonged expression of zinc finger immediate-early gene mRNAs and decreased protein synthesis following kainic acid induced seizures.
Honkaniemi J, Sharp FR
This study examines how seizures affect gene expression and protein synthesis in mouse brain tissue, focusing on immediate-early genes including Nurr1 (NR4A2). It finds that seizure-induced damage leads to prolonged mRNA presence but reduced protein production in specific hippocampal regions. The research suggests these molecular changes may reflect neuronal stress or early signs of cell death pathways.
- Seizures cause prolonged NR4A2 mRNA expression in damaged mouse hippocampus areas.
- Reduced protein synthesis correlates with neuronal damage and cell death in mice.
- NR4A2 appears as one of several immediate-early genes studied, not the primary focus.
- The study uses kainic acid-induced seizures in rodents to model brain injury.
- Findings describe general seizure mechanisms rather than NR4A2-specific genetic syndrome effects.
Nurr1 mRNA expression in neonatal and adult rat brain following kainic acid-induced seizure activity.
Crispino M, Tocco G, Feldman JD, Herschman HR, Baudry M
This study shows that seizure activity rapidly increases Nurr1 mRNA levels in specific regions of the rat brain, with the pattern changing as the animals age. The findings suggest that neuronal activation directly modulates Nurr1 expression and that prolonged induction may relate to why certain neurons are more vulnerable to damage.
- Seizures trigger rapid, transient increases in Nurr1 mRNA in neonatal rat hippocampus.
- Nurr1 induction expands to cortical regions as rats mature after seizure activity.
- Prolonged Nurr1 expression occurs in brain areas susceptible to seizure-induced toxicity.
- Results indicate Nurr1 is modulated by neuronal activity and may influence neuronal vulnerability.
The NGFI-B subfamily of the nuclear receptor superfamily (review).
Maruyama K, Tsukada T, Ohkura N, Bandoh S, Hosono T, Yamaguchi K
This review describes the structural and functional characteristics of the NGFI-B nuclear receptor subfamily, which includes NR4A2 (Nurr1), NOR-1, and NGFI-B. It outlines their roles as immediate-early genes involved in physiological processes and cancer development without identifying specific ligands or clinical treatments.
- NR4A2 belongs to the NGFI-B subfamily of orphan nuclear receptors lacking identified ligands.
- These genes act as immediate-early regulators induced rapidly by various cellular stimuli.
- The review covers structural features, expression patterns, and roles in physiology and oncology.
- No clinical data or treatment implications for NR4A2-related syndromes are presented.
On CNS repair and protection strategies: novel approaches with implications for spinal cord injury and Parkinson's disease.
Olson L, Cheng H, Zetterström RH, Solomin L, Jansson L, Giménez-Llort L, Hoffer BJ, Perlmann T
This review discusses general strategies for central nervous system repair and protection, highlighting the potential of developing ligands that target the Nurr1 transcription factor to protect dopamine neurons in Parkinson's disease. It does not provide specific clinical data or treatment protocols for NR4A2-related syndromes.
- The adult CNS lacks spontaneous regeneration mechanisms for lost nerve cells.
- Nurr1 plays a specific role in the development of dopamine neurons.
- Developing ligands for Nurr1 is proposed as a potential neuroprotective treatment.
- Peripheral nerve bridge grafts are mentioned as a reparative strategy for spinal cord injury.
A divergent role of COOH-terminal domains in Nurr1 and Nur77 transactivation.
Castillo SO, Xiao Q, Kostrouch Z, Dozin B, Nikodem VM
This study identifies a naturally occurring truncated version of the NR4A2 protein (Nurr1a) in mouse brains and demonstrates that removing the C-terminal tail significantly reduces its ability to activate gene transcription. The research highlights functional differences between Nurr1 and the related protein Nur77 regarding how their C-terminal domains influence ligand-dependent activation.
- A truncated NR4A2 isoform, Nurr1a, exists naturally in developing mouse brains.
- Removing just 15 amino acids from the C-terminus reduces transcriptional activity.
- Nur77 responds differently to similar truncations compared to Nurr1.
- The study uses cell culture and mouse models without human data.
Rat nurr1 is prominently expressed in perirhinal cortex, and differentially induced in the hippocampal dentate gyrus by electroconvulsive vs. kindled seizures.
Xing G, Zhang L, Zhang L, Heynen T, Li XL, Smith MA, Weiss SR, Feldman AN, Detera-Wadleigh S, Chuang DM, Post RM
This study identifies the rat version of Nurr1 and shows that its expression in the brain changes rapidly in response to seizures. It confirms that Nurr1 is present in specific memory-related brain areas but does not provide information on human genetics or treatment options for NR4A2 syndrome.
- Researchers isolated the rat Nurr1 gene and confirmed it matches human and mouse versions.
- Nurr1 mRNA is highly expressed in the rat brain, particularly in memory-related cortex areas.
- Seizures trigger a rapid, temporary increase in Nurr1 levels in specific hippocampal cells.
- The study suggests Nurr1 may help process memory but offers no clinical insights for humans.
Expression of zinc finger immediate early genes in rat brain after permanent middle cerebral artery occlusion.
Honkaniemi J, States BA, Weinstein PR, Espinoza J, Sharp FR
This study examines how specific genes respond to brain damage caused by stroke in rats. It finds that several immediate early genes, including Nurr1 (NR4A2), increase their activity in brain regions surrounding the injury site during the first day after the event.
- The study uses a rat model of permanent middle cerebral artery occlusion to simulate stroke.
- Nurr1 mRNA levels rise significantly in the cortex within one hour of induced ischemia.
- Gene expression patterns suggest these changes mark areas of potential delayed neuronal death.
- Findings relate to general brain injury mechanisms rather than NR4A2-related developmental syndromes.
Organization, sequence, chromosomal localization, and promoter identification of the mouse orphan nuclear receptor Nurr1 gene.
Castillo SO, Xiao Q, Lyu MS, Kozak CA, Nikodem VM
This study maps the structure and regulatory elements of the mouse Nurr1 gene to understand how it is turned on. It identifies specific DNA sequences that control gene expression but does not provide information about human disease or treatment options.
- The mouse Nurr1 gene spans 7 kb with eight exons and seven introns.
- Researchers identified two major transcription start sites in the first exon.
- The promoter region contains binding sites for glucocorticoids, cAMP, and c-Jun.
- Findings explain regulatory differences between Nurr1 and the related Nur77 gene.
Functional redundancy of the Nur77 and Nor-1 orphan steroid receptors in T-cell apoptosis.
Cheng LE, Chan FK, Cado D, Winoto A
Nor-1 can take over Nur77's role in triggering T-cell death, showing that these two proteins work together in immune cell regulation, even though they are not directly related to NR4A2-related neurodevelopmental disorders.
- Nor-1 can replace Nur77 in causing T-cell death
- Both proteins act through the same DNA signal
- Nor-1 is activated during immune cell apoptosis
- Function is independent of Fas, a common cell death pathway
- Redundancy suggests potential for compensatory mechanisms
Cloning and structural organization of the gene encoding the murine nuclear receptor transcription factor, NURR1.
Saucedo-Cardenas O, Kardon R, Ediger TR, Lydon JP, Conneely OM
This study maps the physical structure of the Nurr1 gene in mice, identifying its seven exons and promoter region. It provides basic genomic data for research purposes but offers no clinical insights or treatment options for patients.
- The mouse Nurr1 gene spans approximately 6.2 kb with seven exons and six introns.
- The promoter lacks a TATA box but contains GC-rich regions and ATF/CREB binding sites.
- This structural data supports future studies on gene regulation, not clinical care.
- No human genetic variants or patient outcomes are analyzed in this paper.
Neuroendocrine regulation of the hypothalamic pituitary adrenal axis by the nurr1/nur77 subfamily of nuclear receptors.
Murphy EP, Conneely OM
This study shows that Nurr1 and Nur77 proteins directly control the expression of key stress-response genes in pituitary cells. It establishes a molecular mechanism for how these receptors regulate the hypothalamic-pituitary-adrenal axis through specific DNA binding sites.
- Nurr1 and Nur77 bind to promoter regions of CRF and POMC genes.
- These receptors positively regulate POMC expression in pituitary cells.
- Glucocorticoids negatively regulate POMC via the same Nurr1 binding site.
- The study uses primary pituitary cells and cell lines, not human patients.
Retinoid X receptor heterodimerization and developmental expression distinguish the orphan nuclear receptors NGFI-B, Nurr1, and Nor1.
Zetterström RH, Solomin L, Mitsiadis T, Olson L, Perlmann T
This study characterizes the molecular interactions and developmental expression patterns of three related nuclear receptors, including Nurr1 (NR4A2), in the central nervous system. It demonstrates that while Nurr1 and NGFI-B can partner with RXR to regulate gene signaling, Nor1 cannot, suggesting functional redundancy among these proteins during brain development.
- Nurr1, NGFI-B, and Nor1 bind DNA as monomers and activate transcription constitutively.
- Only Nurr1 and NGFI-B form heterodimers with RXR to promote vitamin A signaling.
- Nor1 cannot partner with RXR, distinguishing its signaling pathway from the other two.
- All three receptors show complex, overlapping expression patterns in the developing postnatal brain.
Distribution of messenger RNAs for the orphan nuclear receptors Nurr1 and Nur77 (NGFI-B) in adult rat brain using in situ hybridization.
Xiao Q, Castillo SO, Nikodem VM
This study maps where Nurr1 and Nur77 genes are active in the adult rat brain, showing they occupy different regions despite being related proteins. It provides basic anatomical data on gene expression but offers no insight into human disease mechanisms or treatment options for NR4A2-related syndromes.
- The study uses rats, not humans, to map gene activity in the brain.
- Nurr1 and Nur77 show distinct distribution patterns in adult rat brain regions.
- No clinical data, patient phenotypes, or therapeutic implications are presented.
- Findings describe normal biology rather than disease pathology or treatment.
Cellular expression of the immediate early transcription factors Nurr1 and NGFI-B suggests a gene regulatory role in several brain regions including the nigrostriatal dopamine system.
Zetterström RH, Williams R, Perlmann T, Olson L
This study maps where Nurr1 and NGFI-B proteins appear in developing and adult mouse and rat brains, showing they are present in dopamine-producing areas. It confirms that when dopamine neurons die in these animals, Nurr1 levels drop, linking the gene to dopaminergic health.
- Nurr1 mRNA appears in specific brain regions during development and persists into adulthood.
- Nurr1 co-exists with tyrosine hydroxylase in the substantia nigra of adult rodents.
- Dopamine neuron death causes a corresponding loss of Nurr1 mRNA in animal models.
- Results suggest these transcription factors regulate genes critical for dopamine neuron function.
Effects of phencyclidine on immediate early gene expression in the brain.
Näkki R, Sharp FR, Sagar SM, Honkaniemi J
This study examines how the drug phencyclidine (PCP) affects immediate-early gene expression, including Nurr1, in the brains of animals. It maps the timing and location of this genetic activity to understand potential neurotoxic pathways associated with psychosis-like states. The findings do not provide direct insights into NR4A2-related syndromes or therapeutic options for your child.
- PCP triggers immediate-early gene expression, including Nurr1, in specific brain regions of animals.
- Gene induction shows a biphasic pattern with early and delayed responses in different cortical areas.
- Prolonged gene expression correlates with sites of known PCP-induced neuronal toxicity.
- The study focuses on drug mechanism and neurotoxicity rather than developmental genetics.
Global ischemia induces immediate-early genes encoding zinc finger transcription factors.
Honkaniemi J, Sharp FR
This study shows that brain ischemia triggers the expression of several transcription factors, including Nurr1 (NR4A2), in specific brain regions. It suggests that prolonged expression of these genes may influence whether neurons survive or die after injury.
- Global ischemia induces immediate-early genes like Nurr1 in gerbil brains.
- Nurr1 and other factors appear in hippocampus, cortex, and amygdala after reperfusion.
- Persistent Nurr1 expression correlates with neuronal death in the CA1 region.
- Surviving neurons show different prolonged expression patterns of other transcription factors.
HZF-3, an immediate-early orphan receptor homologous to NURR1/NOT: induction upon membrane depolarization and seizures.
Peña de Ortiz S, Jamieson GA
This study identifies HZF-3 as a protein closely related to NURR1 that activates in response to brain electrical activity and seizures. It demonstrates that HZF-3 binds to DNA similarly to NURR1, suggesting it may work alongside NURR1 to regulate gene expression in the nervous system.
- HZF-3 is a rat protein highly similar to human NURR1.
- HZF-3 expression increases during seizures and membrane depolarization.
- HZF-3 binds to the same DNA target element as NURR1.
- The study suggests HZF-3 regulates genes alongside NURR1 in the brain.
Inhibition of Nur77/Nurr1 leads to inefficient clonal deletion of self-reactive T cells.
Zhou T, Cheng J, Yang P, Wang Z, Liu C, Su X, Bluethmann H, Mountz JD
Inhibiting Nur77/Nurr1 proteins disrupts the normal deletion of self-reactive T cells in the thymus, leading to an accumulation of potentially harmful immune cells. The body compensates for this defect by using alternative pathways in lymph nodes and spleen to maintain tolerance.
- Nur77/Nurr1 inhibition blocks self-reactive T cell deletion in the thymus.
- Self-reactive T cells accumulate significantly in affected mice.
- Tolerance is maintained via Fas-dependent mechanisms in lymph nodes and spleen.
- This study focuses on immune system development, not neurological function.
Comparative distribution of NURR1 and NUR77 nuclear receptors in the mouse central nervous system.
Saucedo-Cardenas O, Conneely OM
This study maps where NURR1 and NUR77 proteins are located in the adult mouse brain to understand their potential roles. It finds that while both proteins appear in some of the same areas, they have distinct overall distribution patterns.
- Researchers mapped NURR1 and NUR77 expression in adult mouse brains using hybridization techniques.
- NURR1 expression is restricted mainly to sensory structures, limbic system, and cerebellum.
- NUR77 expression is widespread throughout the central nervous system.
- The two proteins overlap in specific regions like the limbic system and cerebellum.
- Differential expression suggests distinct regulatory roles for motor function versus cognitive function.
Differential regulation of transcription by the NURR1/NUR77 subfamily of nuclear transcription factors.
Murphy EP, Dobson AD, Keller C, Conneely OM
This study maps how NURR1 and the related protein NUR77 bind to specific DNA sequences to either activate or repress gene transcription. It identifies three new DNA binding sites for these proteins and shows that their opposing effects depend on which site they occupy.
- NURR1 and NUR77 share a common DNA binding motif but exert opposing regulatory effects.
- Three additional specific DNA sequences bind both proteins, one functioning as an enhancer.
- Gene regulation depends on the balance between NURR1 and NUR77 cellular levels.
- Potential target genes include those from neuronal and neuroendocrine origins.
Gene expression of NOR-1, a neuron-derived orphan receptor, is inducible in neuronal and other cell lineages in culture.
Bandoh S, Tsukada T, Maruyama K, Ohkura N, Yamaguchi K
This study shows that NOR-1, a protein closely related to Nurr1, is active in various cell types when stimulated by specific chemical signals. The research demonstrates this induction using cultured rat cells rather than human patients or living animals.
- NOR-1 shares strong sequence similarity with the NR4A2/Nurr1 protein.
- Chemical stimuli induce NOR-1 expression in neuronal, glial, and other cell lines.
- The study uses rat cell cultures, not human subjects or animal models.
- No clinical data or treatment outcomes for NR4A2-related syndromes are presented.
Adrenocortical function and regulation of the steroid 21-hydroxylase gene in NGFI-B-deficient mice.
Crawford PA, Sadovsky Y, Woodson K, Lee SL, Milbrandt J
Mice without the NGFI-B gene (the mouse equivalent of human NR4A2) have normal adrenal function and steroid production, showing that other related proteins can fully compensate. This suggests that NR4A2 is not essential for adrenal hormone production in mice, even though it can regulate key genes in lab studies.
- NR4A2 (NGFI-B) is not required for normal adrenal function in mice
- Other proteins like Nurr1 and SF-1 can take over its role
- Adrenal hormone levels stay normal without NGFI-B
- Stress and ACTH responses remain intact without NGFI-B
- NR4A2 loss does not disrupt steroidogenesis in this model
Unique response pathways are established by allosteric interactions among nuclear hormone receptors.
Forman BM, Umesono K, Chen J, Evans RM
This study reveals that the NR4A2 protein (Nurr1) interacts with RXR to form a new complex that responds to hormones, unlike other nuclear receptors where this partner is inactive. It demonstrates that these molecular partnerships create unique signaling pathways rather than simple combined effects.
- NR4A2 forms a hormone-dependent complex when paired with RXR.
- RXR acts as an active cofactor for NR4A2, not just a passive partner.
- Other receptors like T3R mask RXR's binding properties in heterodimers.
- Allosteric interactions generate diversity in hormone response networks.
A novel pathway for vitamin A signaling mediated by RXR heterodimerization with NGFI-B and NURR1.
Perlmann T, Jansson L
This study defines a molecular mechanism where NURR1 and NGFI-B activate gene expression by partnering with the RXR receptor in response to vitamin A derivatives. It establishes how these orphan receptors shift RXR from an inactive state to an active one, linking retinoid signaling to growth factor pathways.
- NURR1 and NGFI-B heterodimerize with RXR to activate gene expression.
- These pairs bind specific DNA sequences distinct from other RXR partners.
- Vitamin A ligands trigger this activation, shifting RXR to an active state.
- This mechanism links vitamin A signaling to growth factor responses.
Focal brain injury induces multiple immediate early genes encoding zinc finger transcription factors.
Honkaniemi J, Sagar SM, Pyykönen I, Hicks KJ, Sharp FR
This study shows that focal brain injury temporarily increases the expression of Nurr1 (NR4A2) and other immediate early genes in specific brain regions, with levels returning to normal within 24 hours. The findings suggest these transcription factors work together during the brain's response to acute damage.
- Nurr1 expression increases in hippocampal cells after focal brain injury.
- Most induced genes return to baseline levels within 24 hours.
- Egr-3 expression persists longer than other immediate early genes.
- The study uses animal models of brain injury, not human patients.
- No direct link to NR4A2 syndrome treatment or natural history is established.
Three related brain nuclear receptors, NGFI-B, Nurr1, and NOR-1, as transcriptional activators.
Paulsen RF, Granas K, Johnsen H, Rolseth V, Sterri S
This study compares how three related brain proteins activate genes in cell cultures, finding that Nurr1 (NR4A2) has distinct activation capabilities compared to its relatives. The research establishes basic molecular mechanisms of gene regulation without addressing human disease or treatment.
- Researchers tested NGFI-B, Nurr1, and NOR-1 proteins in cultured cells.
- Nurr1 activates specific gene reporters more strongly than NGFI-B.
- Each protein shows unique patterns of gene activation.
- Findings describe general molecular mechanisms in non-human cell lines.
NOT, a human immediate-early response gene closely related to the steroid/thyroid hormone receptor NAK1/TR3.
Mages HW, Rilke O, Bravo R, Senger G, Kroczek RA
This paper identifies NOT (now known as NR4A2) as a human immediate-early gene that is highly expressed in the brain and functions as a transcription factor. It establishes the molecular identity of NR4A2 as the human homolog of murine Nurr1, confirming its role within the steroid/thyroid hormone receptor family.
- NOT is the human homolog of murine Nurr1 and rat RNR-1.
- The gene localizes to chromosome 2q22-q23.
- NOT mRNA expression is strongest in the human brain.
- It acts as an immediate-early response transcription factor.
- It forms a distinct subgroup of orphan steroid receptors.
Induction of multiple immediate early genes in rat hypothalamic paraventricular nucleus after stress.
Honkaniemi J, Kononen J, Kainu T, Pyykönen I, Pelto-Huikko M
Stress rapidly increases the activity of specific genes in a key brain region involved in stress response, including NGFI-A and NGFI-B, which may help regulate how the brain adapts to stress. These genes are not directly related to NR4A2/NURR1 function in neurodevelopment or neurological disorders.
- Stress activates NGFI-A, NGFI-B, fra-2, and TIS11 in the brain's stress center
- These genes are involved in how the brain responds to stress at the genetic level
- NR4A2/NURR1 was not affected by stress in this study
- The findings are from rat brain tissue, not human or NR4A2-related conditions
Endocrine and neurogenic regulation of the orphan nuclear receptors Nur77 and Nurr-1 in the adrenal glands.
Davis IJ, Lau LF
This study maps how stress hormones and nerve signals control the NR4A2 gene in mouse adrenal glands, showing that specific chemical modifications regulate its activity. It provides detailed molecular mechanisms of NR4A2 regulation but does not address brain development or neurological symptoms relevant to your child's syndrome.
- NR4A2 expression in mouse adrenal glands increases under stress stimuli like seizures.
- Hormonal signals activate the gene in adrenal cortex cells via the HPA axis.
- Nerve signals trigger NR4A2 expression in adrenal medulla cells independently of hormones.
- ACTH hormone modifies NR4A2 protein structure to enhance its DNA binding ability.
- The research focuses on peripheral endocrine tissue, not central nervous system function.
Identification of a new brain-specific transcription factor, NURR1.
Law SW, Conneely OM, DeMayo FJ, O'Malley BW
This study identifies and characterizes NURR1 as a brain-specific transcription factor that regulates gene expression in the central nervous system. The research establishes that NURR1 is distinct from related proteins and responds differently to cellular stimuli, highlighting its specific role in brain development.
- Researchers cloned the mouse Nurr1 gene, identifying it as a novel nuclear receptor.
- Nurr1 protein consists of 598 amino acids and shares structural similarities with Nur77.
- Nurr1 expression increases with membrane depolarization but not nerve growth factor stimulation.
- The protein is predominantly found in brain tissue during development and in adults.