Ask about this productRelated genes to: PLSCR3 antibody
- Gene:
- PLSCR3 NIH gene
- Name:
- phospholipid scramblase 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-04
- Date modifiied:
- 2016-11-10
Related products to: PLSCR3 antibody
Related articles to: PLSCR3 antibody
- Immunotherapy efficacy in colorectal cancer (CRC) is largely restricted to microsatellite instability-high (MSI-H) tumors, highlighting an urgent need to overcome resistance in microsatellite-stable (MSS) CRC. Mitochondrial DNA (mtDNA) leakage activates the cGAS-STING pathway, a potent inducer of antitumor immunity. However, endogenous regulators constraining mtDNA release in CRC, particularly within the inner mitochondrial membrane (IMM), remain poorly defined. - Source: PubMed
Publication date: 2026/05/25
Ling LimianWu JingyuBao LeiLiu ZhaohuiDeng QunJi XiaowenYu ShaojunYu FengZhu AkaoXiao QianZheng Wenwen - Acute kidney injury (AKI) continues to pose a significant clinical burden, characterized by high morbidity and mortality rates. Emerging evidence has established mitochondrial dysfunction as a central driver in the pathogenesis of AKI, encompassing deficits in bioenergetics, excessive production of reactive oxygen species, and disruption of mitochondrial dynamics. Therapeutic interventions targeting mitochondrial pathways-most notably peptide-based agents such as SS-31-have demonstrated promising results in preclinical models. Recent discoveries have identified phospholipid scramblase 3 (PLSCR3) as an essential mediator of SS-31's mitochondrial protective effects, positioning it as a novel therapeutic target. This review synthesizes current mitochondrial-directed approaches for AKI, with a particular emphasis on the mechanistic role of PLSCR3 in maintaining mitochondrial homeostasis and injury responses. Despite encouraging data, mitochondrial therapies face several translational hurdles, including limited bioavailability, challenges in establishing effective dosing regimens, incomplete mechanistic understanding, and variability in efficacy across different experimental models. Moreover, concerns regarding cost, accessibility, and long-term safety remain unresolved, contributing to inconsistent outcomes in clinical trials. Herein we evaluate the emerging role of PLSCR3 as a potentially druggable mitochondrial target, supported by recent genetic, biochemical, and in vivo evidence, and discuss translational strategies that may bridge the gap between experimental promise and clinical application. - Source: PubMed
Publication date: 2025/09/29
Patel Prisha SPabla Navjot SBajwa Amandeep - Selective clearance of damaged mitochondria through mitophagy is crucial for the maintenance of mitochondrial homeostasis. While mitophagy can be activated by various mitochondrial toxins, the physiologically relevant signal that triggers mitophagy is less studied. TGFB/TGFβ signaling has been linked to autophagic induction, but its specific role in mitophagy is not well understood. Here, we discovered a novel mitophagy induction paradigm stimulated by TGFB1. The mitophagic response is exclusively mediated by SMAD2, SMAD3, and SMAD4 underlying the TGFB receptor signaling. The transcriptional regulation activates genes involved in the canonical autophagic pathway which is required for the TGFB1-induced mitophagy. Moreover, TGFB1 signaling promotes mitophagic flux by upregulating PLSCR3 that externalizes cardiolipin in conjunction with the MAP1LC3/LC3/GABARAPs-interacting receptor proteins (BNIP3L/NIX, BNIP3, and FUNDC1)-dependent mechanism. Overall, our study characterized the essential components engaged in the TGFB1-induced mitophagy and demonstrated that TGFB is an important signal that induces mitophagy. ATG5: autophagy related 5; ATG8: mammalian homolog of yeast Atg8; ATG9A: autophagy related 9A; ATG13: autophagy related 13; ATG101: autophagy related 101; BNIP3: BCL2 interacting protein 3; BNIP3L/NIX: BCL2 interacting protein 3 like; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; Cardiolipin: 1,3-bis(-3'-phosphatidyl)--glycerol; CERS1: ceramide synthase 1; FUNDC1: FUN14 domain containing 1; GABARAP: GABA type A receptor-associated protein; GABARAPL1: GABA type A receptor-associated protein like 1; GABARAPL2: GABA type A receptor-associated protein like 2; GLS: glutaminase; KO: knockout; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MitoIP: mitochondrial immunoprecipitation; MMP: mitochondrial membrane potential; NRBF2: nuclear receptor binding factor 2; OPTN: optineurin; PINK1: PTEN induced kinase 1; PLSCR3: phospholipid scramblase 3; PRKN: parkin RBR E3 ubiquitin protein ligase; RB1CC1/FIP200: RB1 inducible coiled-coil 1; TGFB/TGFβ: transforming growth factor beta; ULK1: unc-51 like autophagy activating kinase 1. - Source: PubMed
Publication date: 2025/04/01
Yan JiongChen XinChoksi SwatiLiu Zheng-Gang - Diabetic retinopathy (DR) is a major complication of diabetes, leading to severe vision impairment. Understanding the molecular mechanisms, particularly PANoptosis, underlying DR is crucial for identifying potential biomarkers and therapeutic targets. This study aims to identify differentially expressed PANoptosis-related genes (DE-PRGs) in DR, offering insights into the disease's pathogenesis and potential diagnostic tools. - Source: PubMed
Publication date: 2024/12/04
Chen HanChen EnguangCao TingFeng FeifanLin MinWang XuanXu Yu - Cardiolipin (CL), a critical phospholipid situated within the mitochondrial membrane, plays a significant role in modulating intramitochondrial processes, especially in the context of certain cardiac pathologies; however, the exact effects of alterations in cardiolipin on septic cardiomyopathy (SCM) are still debated and the underlying mechanisms remain incompletely understood. This study highlights a notable increase in the expressions of ALCAT1 and PLSCR3 during the advanced stage of lipopolysaccharide (LPS)-induced SCM. This up-regulation potential contribution to mitochondrial dysfunction and cellular apoptosis-as indicated by the augmented oxidative stress and cytochrome c (Cytc) release-coupled with reduced mitophagy, decreased levels of the antiapoptotic protein B-cell lymphoma-2 (Bcl-2) and lowered cell viability. Additionally, the timing of LPS-induced apoptosis coincides with the decline in both autophagy and mitophagy at the late stages, implying that these processes may serve as protective factors against LPS-induced SCM in HL-1 cells. Together, these findings reveal the mechanism of LPS-induced CL changes in the center of SCM, with a particular emphasis on the importance of pathological remodeling and translocation of CL to mitochondrial function and apoptosis. Additionally, it highlights the protective effect of mitophagy in the early stage of SCM. This study complements previous research on the mechanism of CL changes in mediating SCM. These findings enhance our understanding of the role of CL in cardiac pathology and provide a new direction for future research. - Source: PubMed
Publication date: 2024/09/03
Han DongWang ChenyangFeng XiaojingHu LiWang BeibeiHu XinyueWu Jing