ADRA2B
- Known as:
- ADRA2B
- Catalog number:
- 001242A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADRA2B
Related genes to: ADRA2B
- Gene:
- ADRA2B NIH gene
- Name:
- adrenoceptor alpha 2B
- Previous symbol:
- ADRA2L1, ADRA2RL1
- Synonyms:
- ADRARL1
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2015-08-27
Related products to: ADRA2B
Related articles to: ADRA2B
- Frontline caregivers, such as nurses and physicians, face heightened risk of intrusive memories, a core symptom of posttraumatic stress disorder. Understanding intrusions is key to protecting workers' mental health and sustaining effective patient care. Emergency department (ED) staff (N = 331) were assessed before starting ED work and three and six months later. Baseline measures included demographics, prior trauma, cognitive and emotional processing, and polymorphisms of the memory-related NR3C1, KIBRA, and ADRA2B genes as predictors of intrusions at three months, i.e., peak ED stress exposure. We examined intrusion occurrence, frequency, distress, and content, and investigated whether experiencing intrusions moderated changes in mental health from baseline to follow-ups. Intrusions were prevalent and often concerned potential patient care errors. Being a carrier of the G allele of the BCL1 polymorphism of the NR3C1 gene and ruminating were associated with intrusions at three months, while cognitive flexibility, emotional suppression, and emotion-focused positive rumination appeared protective. From baseline to three and six months, participants' anxiety increased, and those experiencing intrusions reported significantly lower work performance and engagement. Our results underline the psychological costs of high-stakes ED settings and suggest improvements to error culture and emotion regulation training as promising avenues to support staff and ultimately patients. - Source: PubMed
Publication date: 2025/12/22
Meine Laura ESchaekel Linda SThörn HannaEhlert UlrikeMaeder Monika BrodmannExadaktylos Aristomenes KBingisser RolandPapassotiropoulos Andreasde Quervain DominiqueGalatzer-Levy IsaacSchultebraucks KatharinaKleim Birgit - Throughout time, there has always been a trend connecting stress and tangible damage to one's physical well-being. However, there's a lack of research that elucidates the physical and molecular traits of this stress on organ integrity. Chronic stress disrupts homeostasis, causing oxidative stress, mitochondrial dysfunction, inflammatory markers, and histological damage. - Source: PubMed
Publication date: 2025/12/22
Asif AbeerBatool RubabArhum ShahzadiAshraf AqsaIqbal Muhammad ZohaibMehmood AzraKlar Agnes SMustafa Muhammad - Structural similarity metrics such as the Tanimoto coefficient (TC) miss many functionally related compounds-indeed, 60% of similarly bioactive ligand pairs in the ChEMBL database show TC < 0.30, revealing a major blind spot that constrains ligand-based discovery. Our motivation is to overcome this blind spot and enable the recovery of structurally different yet functionally equivalent chemotypes that structure-based similarity fails to detect. Here, we introduce the bioactivity similarity index (BSI), a machine learning model that estimates the probability that two molecules bind the same or related protein receptors. Trained under leave-one-protein-out (LOPO) across Pfam-defined protein groups on dissimilar pairs, BSI not only outperforms TC but also surpasses modern molecular embedding baselines (ChemBERTa and contrastive language-molecule pre-training (CLAMP), using cosine similarity) across protein families. We further develop a cross-family model (BSI-Large) that, while slightly below group-specific models, generalizes better and can be fine-tuned with less data, consistently improving over models trained from scratch. In retrospective validation on new ChEMBL v35 data, BSI achieves strong early-retrieval performance (top 2% enrichment factor, EF), with group-specific models delivering the best enrichment, and BSI-Large remaining competitive. In a realistic virtual screening-like scenario against the target gene ADRA2B, the mean rank of the next active, given a known active, improves from 45.2 (TC) to 3.9 (BSI), with 54.9 for ChemBERTa and 28.6 for CLAMP. Altogether, BSI complements, rather than replaces, structure-based similarity and embedding-based comparisons, extending hit finding to remote chemotypes that are structurally dissimilar yet functionally equivalent. The code is available at https://github.com/gschottlender/bioactivity-similarity-index. - Source: PubMed
Publication date: 2025/11/28
Schottlender GustavoPrieto Juan ManuelMarti Marcelo AFernández Do Porto Dario - Mental health problems are highly prevalent worldwide. Stress can precipitate both the onset and recurrence of mental health problems. While many individuals are exposed to similar stressors, there is a large heterogeneity in sensitivity to stress and the extent to which someone subsequently develops mental health issues. A key factor that contributes to an individual's capacity to cope with adversity, referred to as resilience, is genetic variation. Here, we systematically reviewed the effects of genetic variation in the genes encoding the norepinephrine (NE) transporter and receptors on resilience- and mental health-related features in a transdiagnostic approach (i.e., without restrictions regarding factors such as diagnosis or age). Our search yielded 49 studies for inclusion. The current evidence highlights that 1) genetic variations in the NE system (particularly in the and genes) exert influence on some cognitive processes, especially attention and emotional memory; 2) genetic variants in the alpha-2a receptor might play a role in some personality traits; 3) deletion in the and genes seems to be related with altered activity of the amygdala during emotional memory tasks; 4) the link between NE variants and response to methylphenidate are inconclusive. Altogether, these studies provide evidence for a genetic effect of the noradrenergic system in specific resilience- and mental health-related individual characteristics. However, the number of available studies specifically investigating noradrenergic genes were limited, emphasizing the need to perform more research on the noradrenergic system, while taking into account factors such as age, sex, environment, and the potential interactions with other genes. - Source: PubMed
Publication date: 2024/08/06
van Hooijdonk C F MVoulgaropoulou SPodrzaj LWolvekamp Dvan Amelsvoort T A M JLeibold N K - Exercise is a well-recognized non-pharmacological strategy for preventing and managing metabolic dysfunction-associated steatotic liver disease (MASLD, formerly known as NAFLD). While the benefits of exercise are thought to involve epigenetic mechanisms, the precise role of RNA m6A methylation remains unclear. This study investigates how treadmill exercise modulates RNA m6A methylation to prevent MASLD in a high-fat diet (HFD)-induced mouse model. Male C57BL/6 mice were fed either a standard diet (SD) or HFD for 12 weeks, with a subset of HFD-fed mice undergoing treadmill exercise (HFD + Ex). Liver pathology and biochemical markers were assessed. RNA sequencing (RNA-Seq) and methylated RNA immunoprecipitation sequencing (MeRIP-seq) were performed to identify differentially expressed genes (DEGs) and m6A methylation changes. Key candidate gene was validated through siRNA-mediated knockdown in AML-12 cells to assess its role in lipid metabolism. Treadmill exercise alleviated MASLD-related pathology and biochemical abnormalities. RNA-Seq identified 984 DEGs in the HFD vs. SD comparison and 544 in the HFD + Ex vs. HFD comparison. Intersection analysis identified 155 genes upregulated in MASLD and downregulated following exercise. MeRIP-seq revealed 225 hypermethylated and 208 hypomethylated m6A peaks in HFD + Ex vs. HFD groups. Integrative analysis highlighted , , and as key exercise-responsive genes. Silencing through siRNA-mediated knockdown reduced lipid accumulation and suppressed lipogenic gene expression, suggesting its role in exercise-mediated MASLD improvement. Treadmill exercise prevents MASLD by modulating RNA m6A methylation, with emerging as a potential regulator of lipid metabolism. These findings highlight epigenetic modulation as a key mechanism in exercise-induced liver protection. - Source: PubMed
Publication date: 2025/06/17
Liu XueliZhong YuanmingGuo YuqianXu JianhuaWang ShaobingLiu YipingLv YiZheng Xi