Polyclonal Rabbit ARNT2 Antibody
- Known as:
- Polyclonal Rabbit ARNT2 Antibody
- Catalog number:
- KA0289
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ARNT2 Antibody
Related genes to: Polyclonal Rabbit ARNT2 Antibody
- Gene:
- ARNT2 NIH gene
- Name:
- aryl hydrocarbon receptor nuclear translocator 2
- Previous symbol:
- -
- Synonyms:
- KIAA0307, bHLHe1
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-05
- Date modifiied:
- 2015-11-24
Related products to: Polyclonal Rabbit ARNT2 Antibody
Related articles to: Polyclonal Rabbit ARNT2 Antibody
- Certain types of neurons in the central nervous system are wrapped in extracellular matrix protein complexes named perineuronal nets (PNNs). While it is known that PNNs regulate neuronal activity by modulating synaptic plasticity, their pathophysiological role in psychiatric disorders has not been sufficiently clarified. Here, we demonstrate that the expression of PNNs in autism-spectrum-disorder (ASD)-associated mice, valproic acid-injected mice and chromodomain helicase DNA-binding protein 8 (Chd8) gene haploinsufficient mice was decreased in cerebellar nuclei neurons. The pharmacological disruption of PNNs by the enzyme chondroitinase ABC (ChABC) injection into the deep cerebellar nuclei was associated with an impairment of social interaction compared with sham-operated mice. In the large glutamatergic neurons, neuronal activity was increased during social behavior which was revealed by intracellular calcium dynamics and phosphorylation of cAMP responsive element-binding protein 1 (CREB1). The transcriptional factor aryl hydrocarbon receptor nuclear translocator 2 (ARNT2), which regulates neuronal activity, was increased in ChABC-injected mice and ASD-associated mice under the basal condition without any neuronal activity-dependent stimulation of gene expression. Moreover, the evaluation of neuronal activity by the increase of c-Fos in distal regions, including the red nucleus and ventromedial thalamic nuclei, revealed that ChABC injection into the deep cerebellar nuclei negatively affected the c-Fos induction after the social interaction test. The reduction of ARNT2 by injection of adeno-associated virus (AAV) carried shRNA-ARNT2 into the deep cerebellar nuclei, together with ChABC, rescued the impairment of social interaction and restored the induction of c-Fos expression in distal regions compared with scrambled-shRNA-injected mice. Therefore, the present results may imply a functional role of PNNs in the regulation of neuronal activity in the circuits innervated by the cerebellum that orchestrate social behaviour. - Source: PubMed
Publication date: 2026/05/13
Fujita KyotaZhu HongTsuji ChiharuKawamura AtsukiNishiyama MasaakiHigashida HaruhiroYokoyama Shigeru - Tumor initiation and progression frequently involve oncogenic programs that favor proliferation at the expense of lineage commitment and differentiation. Here, we identify a MYC-driven mechanism that suppresses neuronal identity in glioblastoma (GBM) through repression of the transcription factor aryl hydrocarbon receptor nuclear translocator 2 (ARNT2). ARNT2 is highly expressed in the brain, cerebellum, and iPSC-derived neurons but is markedly reduced in GBM tumors and cell lines, where its loss correlates with higher tumor grade and poor survival. Mechanistically, MYC represses ARNT2 expression, and ARNT2 loss results in reduced expression of neuronal and glial identity genes. Although ARNT2 depletion does not alter GBM cell proliferation in vitro, it significantly enhances tumor growth and lipid metabolic remodeling in vivo. Conversely, ectopic ARNT2 expression suppresses tumor burden in both subcutaneous and orthotopic GBM xenograft models and promotes features of neuronal differentiation. Together, these findings identify ARNT2 as a tumor suppressor in GBM and establish MYC-mediated repression of ARNT2 as a critical mechanism by which GBM maintains a proliferative, undifferentiated, stem-like state. - Source: PubMed
Publication date: 2026/05/01
Hao Yi-HengBorenstein-Auerbach NofitGrichuk AnthonyLi LiLafita-Navarro M CarmenFang ShunNogueira Pedro AKim JiwoongXu LinShay Jerry WConacci-Sorrell Maralice - Compared to other amphibians, the Xizang plateau frog, , is the highest elevation-dwelling amphibian species known to date (up to 5,100 m), offering a valuable model for understanding ectotherm adaptation to extreme environments. Here, we compared plasma metabolomes and lung transcriptomes of frogs between higher (4,600 m) and lower (3,400 m) elevations. We also assayed key metabolites (glucose, lactate, NADH, β-hydroxybutyrate) in the plasma and inferred the metabolic flux of central metabolic pathways. - Source: PubMed
Publication date: 2026/01/20
Zhang XuejingNiu YonggangMen ShengkangChen QiangTang Xiaolong - The basic-helix-loop-helix Per-Arnt-Sim (PAS) homology domain (bHLH-PAS) transcription factor (TF) family comprises critical sensors or actuators of physiological (hypoxia, tryptophan metabolites, neuronal activity, and appetite) and environmental (diet-derived metabolites and pollutants) stimuli regulating genes involved in signal adaptation and homeostasis. Despite the importance of this TF family, the mechanisms underlying specificity of DNA binding and target gene regulation by the bHLH-PAS subfamily remain unresolved. We systematically analysed cognate DNA binding hierarchies of prototypical bHLH-PAS family members (ARNT, ARNT2, HIF1α, HIF2α, AhR, NPAS4, SIM1), revealing large DNA binding footprints (12-15 bp) and unique mechanisms of DNA binding specificity involving preferential DNA sequences flanking the core motif. Flank-encoded DNA binding specificity discerns otherwise identical core sequence binding by SIM1 and the HIFs, mediated through N-terminal HIFα-DNA interactions. We also reveal an intimate relationship between DNA shape and core and flank TF binding that allows motif sequence flexibility and underpins multimodal mechanisms for achieving TF binding specificity. Furthermore, novel downstream SIM1 PAS-loop/DNA interactions are associated with AT-rich sequences contributing to DNA binding and transcriptional activity; these interactions are critical for TF biological function underpinning a monogenic cause of human hyperphagic obesity in a recapitulated SIM1.R171H knock-in mouse model. - Source: PubMed
Bersten David CMcDougal Daniel PSullivan Adrienne EGerassimou AlexisBreen JamesFitzsimmons Rebecca LMuscat George E OPederson StephenBruning John BFan Chen-MingThomas Paul QRussell Darryl LPeet Daniel JWhitelaw Murray L - Webb-Dattani syndrome (WEDAS) is an extremely rare autosomal recessive disorder caused by pathogenic variants in the ARNT2 gene. It is characterized by a triad of congenital hypopituitarism, structural brain abnormalities, and multisystem developmental defects. We report the case of a 17-year-old girl with WEDAS who presented with global developmental delay, panhypopituitarism, and arginine vasopressin (AVP) deficiency, formerly known as central diabetes insipidus with adipsia, visual impairment, renal anomalies, and spastic quadriplegia. Her endocrine profile revealed deficiencies in ACTH, TSH, and ADH, and gonadotropins, with a possible growth hormone deficiency. Management included hormone replacement with hydrocortisone, levothyroxine, and desmopressin, as well as fluid regulation and supportive care. Despite multiple hospitalizations due to complications including hypernatremia and infections, the patient survived into adolescence - the longest reported survival in this condition to date - before passing away at age 17. This case expands the known clinical phenotype of WEDAS, emphasizing the importance of early recognition, genetic testing, and a multidisciplinary approach to care for affected individuals, particularly in consanguineous populations where the syndrome may be underdiagnosed. - Source: PubMed
Publication date: 2025/11/25
Alyami Jamilah SalehAlmistehi Wael MohammadAlkanhal Khalid Ibrahim