Ask about this productRelated genes to: PDE4A antibody
- Gene:
- PDE4A NIH gene
- Name:
- phosphodiesterase 4A
- Previous symbol:
- DPDE2
- Synonyms:
- -
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-29
- Date modifiied:
- 2019-04-16
Related products to: PDE4A antibody
Related articles to: PDE4A antibody
- To (1) determine the expression and distribution of all PDE4 isozymes (A-D) along the anterior urethra, (2) culture fibroblasts and epithelial cells from healthy and strictured urethras, (3) investigate an in vitro model of anterior urethral stricture disease (aUSD), and (4) assess the therapeutic potential of phosphodiesterase-4 (PDE4) inhibitors and testosterone compared to paclitaxel. - Source: PubMed
Publication date: 2026/08/06
Lozano Lola PVolk Michael JMiller Carly DBerg Jane EAllamargot ChantalSchlaepfer Charles HKurtzman Jane TChristensen Michael BMyers Jeremy BHertz Alexandria MSwanton Amanda RTucker Budd AErickson Bradley A - Phosphodiesterase 4 (PDE4) facilitates the enzymatic breakdown of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), through its four distinct isotypes, namely PDE4A to PDE4D, along with more than 25 splice variants. It plays a crucial role in cancer development, respiratory issues such as asthma and chronic obstructive pulmonary disease (COPD), autoimmune diseases like psoriasis, and neurological disorders such as Alzheimer's disease. Various methods are being developed to enhance clinical efficacy and reduce side effects. Some of these methods include drug delivery via inhalation and the development of non-emetic PDE4 inhibitors and mixed PDE inhibitors. These inhibitors offer several advantages over traditional formulations, including selectivity for specific inhibitors, targeted tissue distribution, and oral effectiveness. All these efforts have led to the emergence of novel PDE4 inhibitors, with some having progressed to clinical trial stages and others approved as medications. This review summarises PDE4 inhibitors currently in clinical trials, highlighting their therapeutic potential, limitations, and future prospects. - Source: PubMed
Publication date: 2026/07/23
Mailavaram Raghu PrasadChaudhari YogeshS Tarwani RiteshVenugopala Katharigatta NGhosh ManikMaity PrasenjitDeb Pran Kishore - Alcoholic dementia (AlD) is a severe neurological disorder with no effective treatment. Development of pan-phosphodiesterase-4 (PDE4) inhibitors for clinical treatment of neurological conditions has been hampered by emetic side effects primarily mediated by PDE4D, one of the four subtypes of PDE4. Although PDE4A was shown to be upregulated by chronic alcohol exposure, its therapeutic relevance to AlD remains unclear. - Source: PubMed
Tu HuanSun RongzhenMa ShengyaoLi ChunxuLv MingtiHan MeiZhang Han-Ting - Spatially confined β-adrenergic receptor-cAMP nanodomain signaling depends on scaffolded protein-protein interactions (PPIs), yet converting such nanointerfaces into cell-active disruptor peptides remains challenging. Here, we identify a previously unrecognized phosphodiesterase 4A (PDE4A)-filamin A complex in human cardiac tissue that is disrupted in dilated cardiomyopathy. To target this interaction, we developed a nanodomain-resolved AlphaFold3 workflow integrating interface-recurrence filtering, orthogonal docking, and peptide-binding site inference to define a tractable binding region. This approach identified a filamin A docking sequence spanning R2520-H2528, which was optimized to RLVSNHSLH and rendered cell-permeant by N-terminal polyarginine tagging. In ventricular cardiomyocytes, the peptide reduced PDE4A-filamin A proximity and selectively attenuated β-adrenergic cAMP signaling in cytosolic and sarcolemmal compartments, measured by FRET biosensors. This work establishes a potential transferable strategy for translating predicted scaffolded PPI nanointerfaces into functional disruptor peptides and highlights compartmentalized signaling complexes as actionable targets for selective cellular modulation. - Source: PubMed
Lyu SiboJudina AleksandraLing JiayueWright Thomas AKulkarni AditiFu JiarongKibreab IyobelBaillie GeorgeKumar Srivastava PrashantGorelik Julia - Axon regeneration is the key to repairing spinal cord injury. Circadian rhythm plays regulatory roles in axonal regeneration. The endogenous molecular clock serves as the molecular basis for the generation and precise maintenance of circadian rhythms. CLOCK is one of the most core transcription factors in the endogenous molecular clock. However, the role of CLOCK in axon regeneration has so far remained elusive. Therefore, this study explored how the circadian gene clocka regulates the zebrafish central neuronal Mauthner cells (M-cells) axon regeneration. Using the M-cell axonal regeneration model, we found that M-cell axons exhibited circadian-phase-dependent regeneration after two-photon laser ablation, while in the clocka mutant, the circadian-phase-dependent regeneration of M-cells was deprived and their regenerative ability was inhibited. Subsequently, a combination of single-cell electroporation, single-cell capture, transcriptome sequencing, and Rolipram treatment demonstrated that clocka is required for M-cell axonal regeneration and regulates axonal regeneration through phosphodiesterase pde4a-cAMP axis. Together, these findings demonstrate that endogenous molecular clock gene clocka regulates zebrafish central M-cell axonal regeneration via pde4a-cAMP pathway and provide new insights into rhythmic regulation for central nerve repair. - Source: PubMed
Publication date: 2026/06/23
Zhao ZiangHan AlongFan DinggangLi KeqiangZhou JunhuiSong ZhengHu Bing