PRKD1 (phospho-Ser738) Antibody
- Known as:
- PRKD1 (phosphorilated-Ser738) Antibody
- Catalog number:
- abx000203
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- PRKD1 (phospho-Ser738) Antibody
Related genes to: PRKD1 (phospho-Ser738) Antibody
- Gene:
- PRKD1 NIH gene
- Name:
- protein kinase D1
- Previous symbol:
- PRKCM
- Synonyms:
- PKCM, PKD, PKC-mu
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-16
- Date modifiied:
- 2016-10-05
Related products to: PRKD1 (phospho-Ser738) Antibody
Related articles to: PRKD1 (phospho-Ser738) Antibody
- The FOXG1 transcription factor is a crucial regulator of embryonic brain development. Pathogenic FOXG1 variants cause FOXG1 syndrome. Although structural variants in the non-coding region downstream of FOXG1 have been reported in 38 individuals with similar characteristics, the regulatory pathomechanisms remain unknown. Here, we identify two non-coding structural variants in individuals with FOXG1 syndrome-like features, allowing us to delineate a ~ 124 kb commonly affected regulatory region. Using epigenomic profiling and in vivo enhancer assays, we characterize and validate regulatory elements within the commonly affected regulatory region and wider FOXG1 TAD. We see strong activation of previously validated forebrain enhancers, and identify an enhancer cluster and progenitor-specific enhancer region that are strongly activated during forebrain-directed neural progenitor cell differentiation, a process in which FOXG1 is an important regulator. Perturbation of these elements results in varying degrees of reduced FOXG1 transcription in forebrain neural progenitor cells and in population shifts within these cells, while removal of the TAD boundary leads to aberrant expression of the neighbouring PRKD1 gene. Our findings characterize enhancer and architectural elements essential for proper FOXG1 transcription during neurodevelopment, therefore improving variant interpretation in this region. - Source: PubMed
Publication date: 2026/06/03
Hamerlinck LisaD'haene EvaVaughan Michael BVan Loon NorePérez Baca María Del RocíoLeimbacher SebastianKosicki MichaelColombo LaraGenbrugge LukasVantomme LiesDaal EsperanzaRamos Luiza Lorena PiresAvdjieva-Tzavella Daniela MirchevaGoel HimanshuDevriendt KoenJordanova AlbenaDheedene AnneliesVisel AxelMenten BjörnCallewaert BertVergult Sarah - Deterioration of transverse-axial tubules (t-tubules) contributes to insufficient excitation-contraction coupling in heart failure, yet the key signals and mechanisms remain unclear. Here we aimed to identify the signaling pathways that trigger cardiomyocyte t-tubule loss and its underlying cellular process. - Source: PubMed
Publication date: 2026/06/03
Martinez-Vilchez APfeuffer A-K MWeßolowski JFiegle D JAndrä PPotue PKüpfer L KShankar T SSelzman C HDrakos S GHeim CVolk TSeidel T - Impairment in cholesterol uptake and efflux is the main reason contributing to foam cell formation, which is a marker and key step in the atherosclerotic process. Overexpression of long intergenic non-coding RNA-p21 (lincRNA-p21) was reported to alleviate the development of atherosclerosis. However, whether lincRNA-p21 exerts an antiatherogenic function by alleviating lipid metabolism dysfunction and foam cell formation remains unknown. In our study, human THP-1 monocytes were stimulated for 48 h by phorbol 12-myristate-13-acetate (PMA) to differentiate into macrophages, and THP-1-derived macrophages were further treated for 24 h with oxidized low-density lipoprotein (ox-LDL) to differentiate into foam cells. THP‑1 macrophage-derived foam cells were transfected with si-NC/si-lincRNA-p21 or LV-NC/LV-lincRNA-p21 for 48 h to knock down or overexpress lincRNA-p21. lincRNA-p21 expression was reduced in THP-1-derived macrophages after ox-LDL treatment. lincRNA-p21 knockdown promoted lipid uptake and accumulation and inhibited cholesterol efflux in ox-LDL-treated THP-1 macrophages, while lincRNA-p21 overexpression exerted an opposite effect on cholesterol influx and efflux. Importantly, lincRNA-p21 attenuated cholesterol influx by suppressing the PKCδ/Akt/Erk/SR-A/CD36 pathway and enhanced cholesterol efflux by promoting the PPARγ/LXRα/ABCA1/ABCG1 pathway in foam cells derived from THP-1 macrophages. - Source: PubMed
He ChaoYang WeiZhou FeiTeng LinWu HuiGuo ZhuliDing JiawangZhang JingYang JianLi Song - Neuropathic pain is a debilitating chronic condition sustained by maladaptive neuroimmune interactions within the central nervous system, with microglial activation in the spinal dorsal horn serving as a critical driver of pain initiation and chronification. Within this framework, microglial activation mediated by colony-stimulating factor 1 receptor (CSF1R) signaling has emerged as a pathway that is both necessary and sufficient for the development and maintenance of neuropathic pain; however, the upstream mechanisms that determine CSF1R membrane availability and signaling intensity in microglia remain poorly defined. Here, we propose the hypothesis that sphingomyelin synthase 1 (SMS1) functions as a metabolic gatekeeper that amplifies microglial CSF1R signaling by regulating diacylglycerol (DAG)/protein kinase D (PKD)-dependent receptor trafficking. Following peripheral nerve injury, SMS1 expression is upregulated in spinal microglia, leading to increased Golgi-associated DAG production and subsequent PKD activation. Activated PKD promotes vesicular transport of CSF1R from the Golgi apparatus to the plasma membrane, thereby increasing CSF1R surface density and prolonging receptor signaling. Enhanced CSF1R membrane availability amplifies CSF1-driven microglial proliferation and neuroinflammatory signaling, ultimately facilitating synaptic dysregulation and persistent pain hypersensitivity. This hypothesis establishes a direct mechanistic link between sphingolipid metabolism and microglial neuroimmune signaling and identifies SMS1 as a previously unrecognized upstream regulator of neuropathic pain. Targeting SMS1 may therefore represent a novel therapeutic strategy that modulates microglial activation while avoiding the systemic immune suppression associated with direct CSF1R blockade. If validated, this lipid-regulated trafficking mechanism may have broader implications for other microglia-dependent disorders of the central nervous system. - Source: PubMed
Publication date: 2026/04/20
Tan MinghuiWu MeipingWu Meikui - There are four FDA-approved poly (ADP-ribose) polymerase inhibitors (PARPi) for treating metastatic castration-resistant prostate cancer. However, dose-limiting toxicities may reduce efficacy when treatment is de-escalated. Identifying modulators of PARPi sensitivity could enable combination strategies that enhance efficacy while minimizing toxicity. This study investigates whether Protein kinase D1 (PrKD1), recently discovered to modulate DNA repair, influences sensitivity to PARP inhibition. - Source: PubMed
Publication date: 2026/04/17
Shukla SanjeevMcGrath JosephWillis RobertVenkatesh ArjunRodriguez Rosales Reynier DKanumuambidi Jean-PierreMietzsch MarioMcKenna RobertChardon-Robles JonathanBalaji K C