Human ErbB4 _HER4 Protein Vector: HEK294
- Known as:
- Human ErbB4 _HER4 Protein Vector: HEK294
- Catalog number:
- 10015-H01H
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human ErbB4 _HER4 Protein Vector: HEK294
Related genes to: Human ErbB4 _HER4 Protein Vector: HEK294
- Gene:
- ERBB4 NIH gene
- Name:
- erb-b2 receptor tyrosine kinase 4
- Previous symbol:
- -
- Synonyms:
- ALS19, HER4
- Chromosome:
- 2q34
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-07
- Date modifiied:
- 2016-10-05
Related products to: Human ErbB4 _HER4 Protein Vector: HEK294
Related articles to: Human ErbB4 _HER4 Protein Vector: HEK294
- Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder that first manifests in the early stages of childhood. The exact underlying mechanism of ASD remains unknown, and its etiology is rather complex. Neuronal migration, cognitive development, and continuous neural plasticity are strongly influenced by the Neuregulin 1 (NRG1)/ErbB4 signaling pathway. Hence, the pathogenesis of ASD may be closely connected to dysfunction of the NRG1/ErbB4 pathway. According to our current review, either the activation or inhibition of this pathway can lead to the development of ASD, and GABAergic system dysfunction can result in ASD-like behaviors. Moreover, NRG1 binds to ErbB to promote GABA release, and abnormal NRG1 activity affects GABAergic neuron development and function, thus impairing cognition and social interactions. Additionally, the activity of the PI3K/AKT/mTOR pathway differs in various brain regions, and its activation or inhibition can lead to the development of ASD. By activating ErbB CTY-1, NRG1 promotes the development of neurodevelopmental disorders through further activation of the PI3K/AKT/mTOR pathway. Therefore, the NRG1/ErbB4 pathway can regulate GABAergic system functions and affect the activity of the PI3K/AKT/mTOR pathway, thereby resulting in abnormal social interactions and cognitive impairment. Targeting dysfunctions of the GABAergic system, the PI3K/AKT/mTOR pathway, and the NRG1/ErbB4 pathway are currently promising strategies for the treatment of ASD. Candidate agents that modulate these pathways have been shown to be effective in preclinical animal models. However, the limitations of these models and the considerable etiologic and phenotypic heterogeneity among patients with ASD continue to hinder their clinical translation. This article reviews evidence suggesting that the pathogenesis of ASD is closely associated with the NRG1/ErbB4 signaling pathway, the GABAergic system, and the PI3K/AKT/mTOR pathway. This article also analyzes the main obstacles to pharmacological interventions and provides a theoretical basis for understanding the pathogenesis of ASD and for identifying potential targets for future therapeutic strategies. - Source: PubMed
Publication date: 2026/09/21
Du ZiweiMa LipingPeng BingyanShen FenggeWang XianweiZhang Yinghua - The human epidermal growth factor receptor (HER) family is under evaluation as a therapeutic target in urothelial cancer (UC); the significance of expression patterns beyond those of HER2 is unclear. - Source: PubMed
Publication date: 2026/08/05
Coca Membribes SBerney D MBeltran LNally EJackson-Spence FSzabados BMariathasan SPowles TAckerman C - The hypothalamic-pituitary-adrenal (HPA) axis is the central neuroendocrine system that controls physiological stress responses and maintains homeostasis through the coordinated interactions among the hypothalamus, pituitary gland, and adrenal cortex. Dysregulation of the HPA axis is associated with stress-related psychiatric conditions and neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Chronic stress creates a detrimental environment in the brain, inducing structural changes and accelerating brain aging and the loss of neurons. Receptor tyrosine-protein kinase ERBB4 (ERBB4), a member of the epidermal growth factor receptor (EGFR) family, is activated primarily by neuregulin ligands and plays an essential role in neuronal development, synaptic plasticity, and cell survival. Emerging evidence suggests that ERBB4 signaling influences neuroendocrine regulation and stress responsivity. While further studies are needed to provide direct mechanistic evidence linking ERBB4-mediated HPA axis dysregulation to neurodegenerative cell death, this manuscript critically evaluated the preclinical models and proposes a possible feed-forward framework wherein ERBB4 served as a permissive homeostatic modulator at the intersection of stress endocrinology and neuroinflammation. Furthermore, the impact of ERBB4 dysregulation and its mutations on neurodegenerative diseases has been presented, focusing on potential mechanisms of oxidative stress, synaptic dysfunction, and neuronal apoptosis. Taken together, ERBB4 represents an important molecular interface between stress signaling and neurodegenerative pathology. Understanding the regulation of ERBB4 in the HPA axis has provided new insights into the mechanisms underlying neurodegenerative diseases and could identify novel therapeutic targets for stress-associated neurological disorders. - Source: PubMed
Publication date: 2026/09/20
Bagyinszky EvaAn Seong Soo A - Neuroinflammation is a coordinated response to central nervous system injury and disease involving resident glia, neurons, the neurovascular unit, and infiltrating immune cells. Although transient inflammatory signaling supports host defense, debris clearance, and repair, persistent activation contributes to synaptic dysfunction, demyelination, blood-brain barrier disruption, and neuronal loss. Neuregulin-1 (NRG1), a pleiotropic epidermal growth factor family ligand, has emerged as a potential regulator of this balance. Through ErbB receptor complexes, particularly ErbB4-containing dimers, NRG1 influences neural development, myelination, synaptic function, cell survival, and inflammatory signaling. Experimental evidence indicates that NRG1 can restrain NF-κB-dependent transcription, alter microglial activation states, enhance alpha7 nicotinic acetylcholine receptor-associated anti-inflammatory signaling, support oligodendroglial lineage cells, and stabilize neurovascular integrity. However, these actions are context-dependent; in spinal nociceptive circuits, ErbB2-linked signaling can promote microglial activation and pain hypersensitivity. This review examines NRG1 isoform biology, ErbB receptor architecture, cellular targets, and disease-specific evidence across demyelinating disease, stroke, traumatic brain injury, neurodegeneration, cerebral malaria, sickle cell disease, and neuropathic pain. Translation will require isoform-specific, receptor-biased, and anatomically targeted approaches supported by rigorous in vivo validation and verified biomarkers. - Source: PubMed
Publication date: 2026/09/19
Ford Gregory DMcGinley ChristopherOyolola OluwafayokemiAdeyemi OyinkansolaSurles-Zeigler Monique CRahimpour ShokofehFord Byron D - GM1 gangliosidosis is a rare lysosomal storage disorder caused by biallelic mutations in GLB1, leading to progressive neurodegeneration. The cellular and molecular mechanisms, particularly at the neuronal subtype level, remain incompletely understood. - Source: PubMed
Publication date: 2026/09/24
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