Polyclonal Rabbit ADCY5 per 6 Antibody
- Known as:
- Polyclonal Rabbit ADCY5 6 Antibody
- Catalog number:
- KA0104
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ADCY5 per 6 Antibody
Ask about this productRelated genes to: Polyclonal Rabbit ADCY5 per 6 Antibody
- Gene:
- ADCY5 NIH gene
- Name:
- adenylate cyclase 5
- Previous symbol:
- -
- Synonyms:
- AC5
- Chromosome:
- 3q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-22
- Date modifiied:
- 2016-10-18
Related products to: Polyclonal Rabbit ADCY5 per 6 Antibody
Related articles to: Polyclonal Rabbit ADCY5 per 6 Antibody
- Marine fish survival is threatened by ocean acidification, but the hormonal mechanisms for pH compensation are not well understood, limiting mechanistic understanding of stress responses in marine fish. We examined isotocin signaling in marine medaka () exposed to year-2100 ocean acidification conditions (pCO₂ ~0.14 kPa, pH 7.6). Our analysis revealed that isotocin receptor b (ITRb) was selectively upregulated at 6 hours post-exposure in adult gills, though it showed only a non-significant trend at 5 dpf embryos, while adenylyl cyclase 5 (ADCY5) showed hypercapnia responsiveness primarily at hatching. Using immunofluorescence and confocal microscopy, we found that both ITRb and ADCY5 proteins localize to the basolateral membrane of NKA-positive ionocytes, partially separated from apical H⁺-secretion machinery. Knockdown experiments showed that ITRb-ADCY5 coupling is crucial for pH compensation, with individual knockdown moderately reducing H⁺ secretion and combined knockdown causing severe impairment (>70% reduction) and decreasing transcription of acid-secretion genes () by 44-60%. Paradoxically, double knockdown triggered a 2-fold cAMP increase that failed to restore function, whereas wild-type embryos maintained stable cAMP levels across pH conditions, consistent with the hypothesis that ITRb-ADCY5 coupling may organize cAMP production within specific basolateral microdomains, though direct subcellular imaging would be required to validate this compartmentalization model. The developmental asynchrony between ITRb (5 dpf) and ADCY5 (hatching) responses indicates life-stage-specific vulnerabilities. Our findings reveal that basolateral ITRb-ADCY5 coupling represents a critical control point for pH compensation capacity. - Source: PubMed
Publication date: 2026/05/21
Liu Tzu-YenGuh Ying-JeyChen Yi-AnShih Shang-WuChou Pei-HsuanTsou Yi-LinLee Yi-ChunChen Ruo-DongChou Ming-YiLee Jae-SeongHwang Pung-PungHu Marian YTseng Yung-Che - The diagnosis of dystonia is often delayed because of its many different clinical manifestations and causes. Updates to the definition and classification of dystonia can assist clinicians in improving its recognition and timely diagnosis. Dystonia is characterised by sustained or intermittent abnormal movements, postures, or both. Patterned phenomenology, alleviating manoeuvres, worsening by voluntary movement, and overflow to adjacent muscles are all clinical clues of the condition. Additional non-motor manifestations are part of the clinical spectrum. In parallel to the broad heterogeneity of clinical manifestations among different types of dystonia, the biological mechanisms underlying the condition are also heterogeneous. Among these mechanisms, an alteration of the sensorimotor circuits during crucial windows of development might have a role in many forms of dystonia. Advances in the understanding of its pathogenesis indicate that targeting shared mechanisms could provide a treatment approach for multiple types of dystonia, but also suggest the possibility of personalised therapeutic approaches. - Source: PubMed
Roze EmmanuelMcClelland Verity MLange Lara MJinnah Hyder AVidailhet MariePisani Antonio - Advances in genetic testing have allowed for refined phenotypic categorization of pediatric-onset genetic movement disorders. ADCY5-related movement disorder is among this group of conditions for which we have begun to better understand a genotype-phenotype correlation. - Source: PubMed
Publication date: 2026/05/12
DeArias Alexandra LMorrison Peter EVermilion Jennifer A - ADCY5-related movement disorder (ADCY5-RMD) is characterized by axial hypotonia, dyskinesia, and delays in motor development, frequently resulting in hip deformities. Currently, there is limited evidence regarding effective interventions in this population. We report the case of a 30-month-old nonambulatory boy with ADCY5-RMD, presenting with motor delay, hypotonia, and orofacial dyskinesia. Twenty weeks of whole-body vibration therapy (WBVT) with a hip brace was implemented to enhance hip muscle activity and prevent deformity. Hip parameters were assessed via radiography, muscle activity through surface electromyography, and bone metabolism via serum markers. Postintervention, migration percentage, acetabular index, and pelvic obliquity improved. Surface electromyography showed increased peak amplitude in gluteus medius, iliopsoas, and rectus femoris. Although bone mineral density remained unchanged, serum C-terminal telopeptide decreased, indicating bone health benefits. Thus, WBVT with a hip brace may improve muscle activation and reduce hip deformity in ADCY5-RMD, offering a safe, well-tolerated intervention suitable for supervised home use. - Source: PubMed
Publication date: 2026/05/07
Ryu Ju SeokJo Won-JaeChoi HyunjiSuh Jee Hyun - Rodents represent one of the key functional groups in ecosystems, and their population outbreaks can disrupt ecological equilibrium and cause substantial economic losses in agricultural production. Therefore, rational control of rodent populations is essential for maintaining ecosystem stability and minimizing economic damage. The striped hamster displays marked seasonal reproductive patterns, leading to significant fluctuations in population size across seasons. Investigating how female striped hamsters regulate follicle development in response to photoperiodic cues offers a promising target for the strategic management of pest populations. - Source: PubMed
Publication date: 2026/04/16
Xue HuiliangZhang XuetingQi WenFan ChaoXu JinhuiChen LeiWu MingXu Laixiang