Polyclonal Rabbit ADCY4 Antibody
- Known as:
- Polyclonal Rabbit ADCY4 Antibody
- Catalog number:
- KA0102
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ADCY4 Antibody
Related genes to: Polyclonal Rabbit ADCY4 Antibody
- Gene:
- ADCY4 NIH gene
- Name:
- adenylate cyclase 4
- Previous symbol:
- -
- Synonyms:
- AC4
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-22
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit ADCY4 Antibody
Related articles to: Polyclonal Rabbit ADCY4 Antibody
- S-palmitoylation, a reversible lipid-based post-translational modification, is notably elevated in colorectal cancer (CRC) due to common lipid metabolism disorders. It has been reported to play crucial roles in regulating membrane composition, cell proliferation, and metastasis in various malignancies such as pancreatic and breast cancers. However, its role in the progression of CRC remains poorly understood. ZDHHC9, a member of the palmitoyl transferase family, is significantly upregulated in CRC patients and correlates with poor prognosis. Knockdown of ZDHHC9 impairs CRC cell proliferation and migration both in vitro and in vivo. RNA sequencing revealed that ZDHHC9 depletion markedly downregulates the cAMP signaling pathway. Mechanistically, ZDHHC9 knockdown impairs ADCY4 activity by reducing S-palmitoylation of KLF5 at cysteine 438, thereby modulating the ZDHHC9/KLF5/ADCY4 axis and downstream cAMP/PKA/CREB signaling to influence CRC cell proliferation and migration. Our findings demonstrate that ZDHHC9 promotes CRC progression by regulating intracellular cAMP levels through KLF5 palmitoylation, providing a novel therapeutic perspective targeting palmitoylation in CRC. The mechanism diagram of this study. ZDHHC9 mediates palmitoylation of KLF5 at cysteine 438, thereby enhancing ADCY4 activity and increasing intracellular cAMP levels. This elevation in cAMP promotes PKA and phosphorylation of CREB, ultimately activating the cAMP/PKA/CREB signaling pathway, which contributes to the regulation of CRC cell proliferation, migration, and resistance to 5-FU. (Created with BioRender.com). - Source: PubMed
Publication date: 2026/03/25
Zhang HaoTian YuanXiang ZeyuHan FengChen MiaomiaoJiang ChunhuiLiu YeXue HanbingHu LipengXu ChunjieGu LeiXu Qing - Adenylate cyclase 4 (ADCY4), a member of the adenylate cyclase family, is an enzyme responsible for catalyzing the synthesis of the secondary messenger cyclic adenosine monophosphate (cAMP). Emerging evidence suggests a potential link between ADCY4 expression and the prognosis as well as biological behaviors of specific malignancies. Nevertheless, a systematic investigation into the role of ADCY4 in pan-cancer prognosis and its regulatory influence on the tumor microenvironment remains insufficient. - Source: PubMed
Publication date: 2026/03/17
Yu CuiFang LiuMeijuan CaiYuanli WangMin Fang - Colorectal cancer (CRC) is increasingly diagnosed in individuals under 50 years of age, yet the underlying genetic predisposition remains largely unexplained, particularly in mismatch repair (MMR)-proficient cases. This study aimed to identify novel hereditary CRC susceptibility genes by integrating germline and tumour whole-exome sequencing (WES) with transcriptomic profiling across a cohort of early-onset CRC (EOCRC) patients. Tumours were categorised using Consensus Molecular Subtypes (CMS) classification and analysed for mutational signature and burden. We used a novel 'All vs One' multi-omic integration approach to identify loss-of-function rare germline variants with concordant gene expression alterations in tumour tissue. Five candidate genes (ADCY4, NOXO1, CDHR2, ARHGAP10, EEF2K) were prioritised based on this approach and potential biological relevance in CRC. These findings highlight the molecular heterogeneity of EOCRC and demonstrate the utility of multi-omic approaches in refining germline variant interpretation. Integrating tumour transcriptomics enhances gene discovery efforts and supports a more comprehensive understanding of CRC heritability in younger individuals. - Source: PubMed
Publication date: 2026/01/15
López-Novo AnaelAmigo JorgeDacal AndrésRemedios-Espino DavidCubiella JoaquínÁlvarez-Sánchez María VictoriaLadra-González María JesúsFernández-López FernandoÁlvarez-Castro AnaCarlés SilviaCameselle-Teijeiro José ManuelCuatrecasas MiriamBalaguer FrancescCastellví-Bel SergiFernández-Rozadilla CeresCarracedo ÁngelRuiz-Ponte Clara - BackgroundPrevious whole exome and whole genome sequencing (WES/WGS) studies identified genome-wide significant associations for late-onset Alzheimer's disease (AD) with rare variants but highlighted the need for larger samples.ObjectiveIdentify associations of rare coding variants with AD risk in a large-scale, multi-ancestry exome-wide.MethodsWe combined non-overlapping portions of the Alzheimer's Disease Sequencing Project (ADSP) WES (n = 18 717) and WGS (n = 35 014) datasets obtaining a sample (n = 34 202) including participants ages ≥ 60 from four genomic similarity clusters consistent with European ancestry (EA, 9 744 AD cases and 9 095 controls), African American (AA, 1 944 AD cases and 4 215 controls), Caribbean Hispanic (CH 2 344 AD cases and 3 465 controls), and Native American Hispanic (NAH 743 AD cases and 2 652 AD controls) populations. Association of AD with 253,421 bi-allelic variants with minor allele count ≥ 20 in the total sample and each population group was evaluated using GENESIS. Gene-based tests comprising predicted moderate and high-impact variants were performed using SAIGE.ResultsNovel study-wide significant associations (p < 1.97 × 10) were identified with variants enriched among the Amish in (rs927193859, p = 1.58 x10), (rs150289554, p = 8.60 × 10), and (rs140218057, p = 1.77 × 10) in the total sample. Population-specific analyses confirmed significant associations with in all groups and detected an association in CH individuals with the missense mutation G206A (p = 3.07 × 10), a variant that was previously linked to early-onset AD in Hispanics. Gene-based tests highlighted significant associations with (p = 2.75 × 10), (p = 2.80 × 10), and (p = 7.43 × 10).ConclusionsWe identified rare variants in novel genes which provide new insights into AD pathogenesis. - Source: PubMed
Publication date: 2025/12/22
Khurshid ZainabFarrell John JTong TongZhu Congcong Martin Eden RBush WillPericak-Vance Margaret AWang Li-SanSchellenberg GerardHaines Jonathan LLunetta Kathryn LLeung Yuk YeeZhang XiaolingFarrer Lindsay A - A primary hallmark of pathological cardiac hypertrophy is excess protein synthesis due to enhanced translational activity. However, regulatory mechanisms at the translational level under cardiac stress remain poorly understood. Here we examined the translational regulations in a mouse cardiac hypertrophy model induced by transaortic constriction (TAC) and explored the conservative networks the translatome pattern in human dilated cardiomyopathy (DCM). The results showed that the heart weight to body weight ratio was significantly elevated, and the ejection fraction and fractional shortening significantly decreased 8 weeks after TAC. Puromycin incorporation assay showed that TAC significantly increased protein synthesis rate in the left ventricle. RNA-seq revealed 1,632 differentially expressed genes showing functional enrichment in pathways including extracellular matrix remodeling, metabolic processes, and signaling cascades associated with pathological cardiomyocyte growth. When combined with ribosome profiling analysis, we revealed that translation efficiency (TE) of 1,495 genes was enhanced, while the TE of 933 genes was inhibited following TAC. In DCM patients, 1,354 genes were upregulated 1,213 genes were downregulated at the translation level. Although the majority of the genes were not shared between mouse and human, we identified 93 genes, including , , , , , , etc., with highly conserved translational regulations. These genes were remarkably associated with myocardial function, signal transduction, and energy metabolism, particularly related to cGMP-PKG signaling and fatty acid metabolism. Motif analysis revealed enriched regulatory elements in the 5' untranslated regions (5'UTRs) of transcripts with differential TE, which exhibited strong cross-species sequence conservation. Our study revealed novel regulatory mechanisms at the translational level in cardiac hypertrophy and identified conserved translation-sensitive targets with potential applications to treat cardiac hypertrophy and heart failure in the clinic. - Source: PubMed
Wang Bao-SenLyu JianZhan Hong-ChaoFang YuGuo Qiu-XiaoWang Jun-MeiLi Jia-JieXu An-QiMa XiaoGuo Ning-NingLi HongWang Zhi-Hua