Ask about this productRelated genes to: PCDGF antibody
- Gene:
- GRN NIH gene
- Name:
- granulin precursor
- Previous symbol:
- -
- Synonyms:
- PCDGF, PGRN, CLN11
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-30
- Date modifiied:
- 2019-04-23
Related products to: PCDGF antibody
Related articles to: PCDGF antibody
- Accumulating evidence indicates that crosstalk between immune cells and intrinsic cochlear cells is critical for maintaining auditory homeostasis. However, the activation profile of cochlear microglia-like cells (MLCs) and their mechanistic role in age-related hearing loss (ARHL) remain poorly defined. Here, we show that MLCs are robustly activated in the cochlea of aged mice, and that pharmacologic depletion of cochlear MLCs significantly attenuates ARHL progression. To dissect the mechanisms underlying MLC-driven cochlear damage in ARHL, we leveraged the single-cell transcriptomic landscape of the aged mouse cochlea previously generated by our research group, and conducted the related functional validation. We identified prominent age-related alterations in cochlear MLCs, and revealed that AAV-mediated (via posterior semicircular canal microinjection) upregulation of progranulin (GRN) in MLCs mitigates aging-associated oxidative stress damage in the cochlea. Collectively, our work demonstrates that targeting GRN signaling in cochlear MLCs alleviates aging-related oxidative stress in the cochlea, and thereby delays ARHL progression. - Source: PubMed
Publication date: 2026/08/06
Li QiLiu MengxiaoYin HuanCao HuanWang JiantaoYang JianwangLiu TaoWang Baoshan - Outcomes with sirolimus-coated drug-eluting balloons (DEB) have been positive for the treatment of femoropopliteal arterial lesions but have not been studied in a broader patient population. - Source: PubMed
Publication date: 2026/08/08
Lichtenberg MichaelZeller ThomasPatel AshishKickuth RalphPascua Julio AndrésSchmehl JörgHertting KlausKatsanos KonstantinosOberacker RalphRastan AljoschaMüller-Hülsbeck StefanGissler Hans-MartinKorosoglou GrigoriosHeiss ChristianRammos Christos - Animal traits develop through intricate patterns of gene expression that are regulated at multiple levels. This regulation includes interactions between transcription factors and cis-regulatory element (CRE) DNA sequences, and the dynamic accessibility of CREs due to chromatin modifications and remodeling. Polycomb Group (PcG) and Trithorax Group (TrxG) genes are evolutionarily conserved regulators of chromatin state. Although the PcG and TrxG genes have well understood roles in developmental gene regulation, the extent to which these complexes contribute to trait evolution remains unclear. Here, we performed a genetic screen to understand how PcG and TrxG genes shape the rapidly evolving gene regulatory network (GRN) responsible for the dimorphic abdomen tergite pigmentation of Drosophila (D.) melanogaster fruit flies. A near-comprehensive screen of TrxG and PcG genes was conducted using RNAi, and numerous genes were identified whose reduced expression caused alterations to tergite pigmentation. For the eight most impactful genes, their roles in regulating this GRN were explored. We assessed their effects on several key transcription factors, and downstream CREs that are responsible for the expression of the GRN's pigmentation enzyme genes. We show that multiple members of the PcG and TrxG complexes are required for distinct tiers in the pigmentation GRN, suggesting potential points where responsive elements for different factors may have evolved. The results set the stage for future studies to identify the direct GRN targets of PcG and TrxG complexes, and how they have participated in the evolution of this GRN. - Source: PubMed
Publication date: 2026/08/07
Seibert Devon MWilliams Ashley VRanly Madeline AWilliams Melissa EKonys Claire CWeinstein Michael LRock Jenna RStanojev Rachel MStone Corinne RDaniel Emily BWilliams Eliana GRebeiz MarkWilliams Thomas M - Mutations in progranulin gene (GRN) are a major cause of frontotemporal dementia (FTD). Most reported pathogenic mutations are nonsense, frameshift, or splicing mutations, resulting in a premature stop codon, degradation of mutated mRNA and consequent protein haploinsufficiency. - Source: PubMed
Publication date: 2026/04/04
Ricci MDi Fede GCaroppo PAprea VVilla CRomeo ATiraboschi PMarti AGrisoli MPiccione M MCimini SRossi Giacomina - Dementia is a syndrome caused by various diseases including Alzheimer's disease (AD) and frontotemporal dementia (FTD) with an estimated global prevalence of 60 million individuals. Recently, therapeutic development in the dementia field has accelerated, with the introduction of monoclonal antibody therapeutics such as Lecanemab and Donanemab. However, AD and FTD patients are still either diagnosed too late to benefit from available therapies or are misdiagnosed due to the clinical overlap between dementia subgroups making therapeutic intervention challenging. This highlights a real need to improve early diagnostic tools of neurodegenerative disease (ND) biomarkers. A potential source of such biomarkers come from small extracellular vesicles (sEVs), groups of cell-derived, lipid-bound assemblies with the capability to cross the blood-brain barrier (BBB) and known to carry pathogenic proteins associated with AD and FTD. A known cargo of sEVs is microRNA (miRNA), regulatory molecules that post-transcriptionally silence gene expression including transcripts of autophagic systems, processes which dysfunction in dementia-causing diseases leading to toxic aggregate build-up, causing neurodegeneration. The targeting of functional machineries in macroautophagy (MA) and chaperone-mediated autophagy (CMA) by different miRNA may vary between AD and FTD mutations, leading to potential biomarkers of disease being highlighted. Through isolating sEVs from the frontal cortex of post-mortem brain tissue of AD, FTD-, FTD-, FTD- and no-disease control patients (Manchester Brain Bank), miRNA cargoes were analysed and compared using real-time quantitative PCR (RT-qPCR). Seven autophagy-associated miRNA candidates (MA: miR-124-3p, miR-30a-5p, miR-128-3p; and CMA: miR-224-5p, miR-373-5p, miR-106a-3p and miR-26b-5p) were tested to identify dementia sub-group variations, used alongside small RNA-sequencing to explore broader miRNA variation within sEV populations. Of the miRNA tested miR-224-5p ( = 1.76 × 10) and miR-106a-3p ( = 0.033) showed significant group differences, and further significant pairwise comparison differences [miR-224-5p: AD fold change (FC) = 4.29, MAPT FC = 7.62; miR-106a-5p: AD FC = 5.59] when compared with no disease controls and other dementia subgroups, potentially showing initial diagnostic and differentiating potential. Small RNA-sequencing results revealed 8 AD, 2 FTD-, 52 FTD- and 12 FTD- differentially expressed sEV-miRNAs when compared with no disease controls. Further direct comparisons between AD versus FTD mutation-derived sEV cargoes, and even FTD mutation versus FTD mutation-derived sEV cargoes, identified additional miRNA with differentiating capabilities. These findings demonstrate sEV-derived miRNA signatures vary across dementia sub-types and suggest potential roles of sEV cargoes in both disease diagnostics and identifying drivers of ND, such as autophagic impairments and signalling pathways. - Source: PubMed
Publication date: 2026/07/21
Morgan JosephAarons TobyMukhopadhyay ArijitLace Gemma