Ask about this productRelated genes to: PPP6R1 Blocking Peptide
- Gene:
- PPP6R1 NIH gene
- Name:
- protein phosphatase 6 regulatory subunit 1
- Previous symbol:
- KIAA1115, SAPS1
- Synonyms:
- SAP190
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-10
- Date modifiied:
- 2015-11-18
Related products to: PPP6R1 Blocking Peptide
Related articles to: PPP6R1 Blocking Peptide
- Environmental endocrine-disrupting chemicals (EDCs) are increasingly implicated in male infertility, yet the gene-level mechanisms by which EDCs contribute to non-obstructive azoospermia (NOA) remain unclear. This study aimed to identify EDC-related genes that are causally linked to NOA and uncover their potential roles in reproductive dysfunction. - Source: PubMed
Publication date: 2025/09/16
Hong YanggangWang YirongLi JiajunShu WanyiChen HaolinChen Congde - The innate immune system serves as the first line of host defense. Transforming growth factor-β-activated kinase 1 (TAK1) is a key regulator of innate immunity, cell survival, and cellular homeostasis. Because of its importance in immunity, several pathogens have evolved to carry TAK1 inhibitors. In response, hosts have evolved to sense TAK1 inhibition and induce robust lytic cell death, PANoptosis, mediated by the RIPK1-PANoptosome. PANoptosis is a unique innate immune inflammatory lytic cell death pathway initiated by an innate immune sensor and driven by caspases and RIPKs. While PANoptosis can be beneficial to clear pathogens, excess activation is linked to pathology. Therefore, understanding the molecular mechanisms regulating TAK1 inhibitor (TAK1i)-induced PANoptosis is central to our understanding of RIPK1 in health and disease. - Source: PubMed
Publication date: 2024/05/29
Bynigeri Ratnakar RMalireddi R K SubbaraoMall RaghvendraConnelly Jon PPruett-Miller Shondra MKanneganti Thirumala-Devi - Sudden cardiac death due to ventricular fibrillation (VF) during ST-elevation acute myocardial infarction (STEAMI) significantly contributes to cardiovascular-related deaths. Although VF has been linked to genetic factors, variations in copy number variation (CNV), a significant source of genetic variation, have remained largely unexplored in this context. To address this knowledge gap, this study performed whole exome sequencing analysis on a cohort of 39 patients with STEAMI who experienced VF, aiming to elucidate the role of CNVs in this pathology. The analysis revealed CNVs in the form of duplications in the and genes as well as CNVs in the form of deletions in the and genes, which could potentially serve as risk indicators for VF during STEAMI. The analysis also underscores notable CNVs with an average gene copy number equal to or greater than four in , , , , , and genes. These findings provide further insight into the role of CNVs in VF in the context of STEAMI. - Source: PubMed
Publication date: 2024/02/22
Lorente-Bermúdez RobertoPan-Lizcano RicardoNúñez LucíaLópez-Vázquez DomingoRebollal-Leal FernandoVázquez-Rodríguez José ManuelHermida-Prieto Manuel - Adipose-derived stem cells (ADSCs) are used in tissue regeneration therapies. The objective of this study is to identify stable reference genes (RGs) for use in gene expression studies in a characterized equine adipose-derived mesenchymal stem cell (EADMSC) differentiation model. ADSCs were differentiated into adipocytes (ADs) or osteoblasts (OBs), and the proteomes from these cells were analyzed by liquid chromatography tandem mass spectrometry. Proteins that were stably expressed in all three cells types were identified, and the mRNA expression stabilities for their corresponding genes were validated by RT-qPCR. , , and then either or demonstrated the most stable mRNA levels. Normalizing target gene C data with at least three of these RGs simultaneously, as per MIQE guidelines ( and with either or ), resulted in congruent conclusions. expression was increased in ADs (5.99 and 8.00 fold, = 0.00002 and = 0.0003) and in OBs (5.18 and 5.91 fold, = 0.0011 and = 0.0023) relative to ADSCs. expression was slightly higher in ADs relative to ADSCs (1.97 and 2.65 fold, = 0.04 and = 0.01), but not in OBs (0.9 and 1.03 fold, = 0.58 and = 0.91). - Source: PubMed
Publication date: 2023/03/08
Riveroll Angela LSkyba-Lewin SabrinaLynn K DevonMubyeyi Glady'sAbd-El-Aziz AhmadKibenge Frederick S TKibenge Molly J TCohen Alejandro MEsparza-Gonsalez BlancaMcDuffee LaurieMontelpare William J - Cellular responses to DNA damage include activation of DNA-dependent protein kinase (DNA-PK) through, among others, the serine/threonine protein phosphatase 6 (PP6). We previously showed that recognition of DNA-PKcs is mediated by the SAPS1 PP6 regulatory subunit. Here, we report and characterize a SAPS1 null mouse and investigate the effects of deletion on DNA damage signaling and repair. Strikingly, neither SAPS1-null animals nor cells derived from them show gross defects, unless subjected to DNA damage by radiation or chemical agents. The overall survival of SAPS1-null animals following whole body irradiation is significantly shortened as compared to wild-type mice, and the clonogenic survival of null cells subjected to ionizing radiation is reduced. The dephosphorylation of DNA damage/repair markers, such as γH2AX, p53 and Kap1, is diminished in SAPS1-null cells as compared to wild-type controls. Our results demonstrate that loss of SAPS1 confers sensitivity to DNA damage and confirms previously reported cellular phenotypes of SAPS1 knock-down in human glioma cells. The results support a role for PP6 regulatory subunit SAPS1 in DNA damage responses, and offer a novel target for sensitization to enhance current tumor therapies, with a potential for limited deleterious side effects. - Source: PubMed
Publication date: 2019/11/09
Dziegielewski JaroslawBońkowska Magdalena APoniecka Ewa AHeo JinhoDu KangpingCrittenden Rowena BBender Timothy PBrautigan David LLarner James M