Ask about this productRelated genes to: PDE3B antibody
- Gene:
- PDE3B NIH gene
- Name:
- phosphodiesterase 3B
- Previous symbol:
- -
- Synonyms:
- HcGIP1
- Chromosome:
- 11p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-02
- Date modifiied:
- 2015-11-18
Related products to: PDE3B antibody
Related articles to: PDE3B antibody
- Sepsis remains a critical global health challenge characterized by high mortality and morbidity, primarily due to the limitations of current pathogen-centric therapies and a poor understanding of host-defense mechanisms. This review synthesizes the pivotal role of the adipose-immune-metabolic axis as a central regulator of disease tolerance-a host defense strategy that limits tissue damage without directly reducing pathogen load. We delineate how adipose tissue is reprogrammed from a passive energy reservoir into an active immunometabolic hub during sepsis. This functional shift is governed by three core hypotheses: "Metabolic Defense Priority," which describes the preferential mobilization of fat to spare skeletal muscle protein; "Bidirectional Immunometabolic Crosstalk," wherein immune cells such as macrophages and B cells precisely regulate lipolysis via specific cytokine signals (e.g., IL-1β and TGF-β); and "Stage-Specific Adaptation," which outlines the dynamic evolution of axis function from the acute to chronic phases of sepsis. We further dissect key molecular pathways, including the Insulin-INSR-Thermogenesis, TGFβ-PDE3b-cAMP, and STING-ER Stress-mtROS axes, that orchestrate this complex interplay. Finally, we discuss contemporary challenges in mechanistic understanding, model translatability, and clinical translation, while proposing future directions to leverage this axis for developing novel, tolerance-based therapeutic strategies to improve sepsis outcomes. - Source: PubMed
Publication date: 2026/03/03
Du QuanyueHe FanghaoZhang ShanchiLan XiongyanPan YanqiuWang Jiajun - The cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling pathway plays a central role in adrenal function, steroidogenesis, and blood pressure regulation. Increasing evidence suggests that dysregulation of this pathway contributes to several forms of hypertension, both endocrine and non-endocrine. A growing number of germline and somatic alterations affecting components of the cAMP/PKA axis have been implicated as key drivers of hypertensive disorders. Among these, activating pathogenic variants (PV) in , which encodes the stimulatory G protein α-subunit (Gsα) responsible for cAMP production, have been linked to cortisol excess. Mosaic PV , which may present with ACTH-independent Cushing syndrome, while somatic PV have been identified in cortisol-producing adrenal adenomas. Germline inactivating variants in are associated with Furthermore, germline alterations in phosphodiesterases such as and , which impair cAMP degradation, have been associated with Cushing syndrome and micronodular adrenal hyperplasia. Somatic activating PV in , the gene encoding the catalytic subunit of PKA, have also been described in cortisol-producing adenomas. In primary aldosteronism, recent studies-including data from our group-suggest that germline variants in and may contribute to bilateral adrenal hyperplasia and autonomous aldosterone production by modulating intracellular cAMP levels. Additionally, gain-of-function PV in have been associated with a familial form of salt-independent hypertension characterized by enhanced PKA signaling and vascular remodeling. This expanding body of evidence underscores the critical role of the cAMP/PKA pathway in the pathophysiology of distinct hypertensive phenotypes and highlights novel molecular mechanisms and potential therapeutic targets that merit further investigation. - Source: PubMed
Publication date: 2026/02/24
Lima Sobrinho Jose Antonio BAlmeida Madson Q - Osteoclastogenesis-associated transmembrane protein 1 (OSTM1) is a membrane-integral glycosylated protein known for regulating lysosomal homeostasis, with loss-of-function mutations causing autosomal recessive osteopetrosis. Through a whole-genome CRISPR/Cas9 screen, we identified OSTM1 as a critical tumor suppressor in B-cell malignancies. In humans, OSTM1 is frequently deleted or downregulated across a wide range of B-cell malignancies. In mice, B-cell-specific monoallelic or biallelic ablation cooperates with loss to drive lymphomagenesis with near 100% penetrance. Mechanistically, we reveal that a cytosolic, non-glycosylated fraction of OSTM1 functions as an E3 ligase that targets phosphodiesterase 3B (PDE3B) for proteasomal degradation. Because PDE3B catalyzes the conversion of cAMP to AMP and thereby negatively regulating the cAMP-dependent PKA/CREB/CREBBP tumor suppressive pathway, the loss of OSTM1 leads to PDE3B stabilization and enhanced cell transformation. Our findings establish OSTM1 as a pivotal E3 ligase that prevents B-cell lymphomagenesis through the regulation of the cAMP/PKA/CREB pathway. - Source: PubMed
Publication date: 2026/01/26
Tariq Muhammad UsamaSheshadri NamrathaShen JianliangJung JaeyongLi RongrongLu KevinYan JunrongKoch Mark CCaso GiuseppeSajjad HassanVallat BrindaBurley Stephen KSun YiLiu TongLi HongHinrichs ChristianBertoni FrancescoLin Richard ZWang JunWang Y LynnVacher JeanXie PingZong Wei-Xing - Thoracic aortic aneurysm (TAA) is driven by complex molecular mechanisms beyond size thresholds, yet the role of cyclic nucleotide metabolism remains unclear. Phosphodiesterases (PDEs), which hydrolyze cAMP and cGMP in compartmentalized microdomains, act as key regulators of vascular integrity and remodeling. - Source: PubMed
Publication date: 2026/01/01
Magouliotis Dimitrios ESicouri SergeAndroutsopoulou VasilikiBaudo MassimoCabrucci FrancescoZotos Prokopis-AndreasXanthopoulos AndrewRamlawi Basel - Genome-wide association studies (GWAS) at biobank scale are computationally intensive, especially for admixed populations requiring robust statistical models. SAIGE is a widely used method for generalized linear mixed-model GWAS but is limited by its CPU-based implementation, making phenome-wide association studies impractical for many research groups. - Source: PubMed
Rodriguez AlexKim YoungdaeNandi Tarak NathKeat KarlKumar RachitConery MitchellBhukar RohanLiu MoleiHessington JohnMaheshwari Ketan Begoli EdmonTourassi GeorgiaMuralidhar SumitraNatarajan PradeepVoight Benjamin FCho KellyGaziano John MichaelDamrauer Scott MLiao Katherine PZhou WeiHuffman Jennifer EVerma AnuragMadduri Ravi K