PLSCR1 (rat)
- Known as:
- PLSCR1 (rat)
- Catalog number:
- 21-495-R100
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- PLSCR1 (rat)
Related genes to: PLSCR1 (rat)
- Gene:
- PLSCR1 NIH gene
- Name:
- phospholipid scramblase 1
- Previous symbol:
- -
- Synonyms:
- MMTRA1B
- Chromosome:
- 3q24
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-08
- Date modifiied:
- 2016-10-05
- Gene:
- SRRT NIH gene
- Name:
- serrate, RNA effector molecule
- Previous symbol:
- -
- Synonyms:
- Asr2, serrate, ARS2
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2009-03-02
- Date modifiied:
- 2016-10-05
Related products to: PLSCR1 (rat)
α - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS:(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2 Related articles to: PLSCR1 (rat)
- The human genome encodes thousands of long non-coding RNAs (lncRNAs) that regulate innate immunity and viral life cycles, yet their roles in viral entry remain understudied. Here, we conducted a genome-wide CRISPR interference screen to identify lncRNAs that regulate SARS-CoV-2 entry. We identified two lncRNAs that modulate angiotensin-converting enzyme 2 (ACE2) dependent viral entry through distinct mechanisms. Our findings suggest that the RP11-314A20.5 locus acts as a -regulatory element that modulates the expression of neighboring genes, including MED11 and CXCL16, linking this genomic region to host pathways associated with SARS-CoV-2 entry and COVID-19 severity. In contrast, CNPY2-AS1 functions in trans as a central regulator coupling cellular redox homeostasis to innate immune signaling. Mechanistically, CNPY2-AS1 associates with thioredoxin reductase 1 (TXNRD1), a key enzyme that limits reactive oxygen species. Loss of CNPY2-AS1 disrupts redox balance, triggering ligand-independent STAT1 activation and IRF7-mediated interferon and inflammatory responses. This dysregulated program has dual effects: induction of the interferon-stimulated gene PLSCR1 restricts viral entry by reducing cell-surface ACE2, while concurrent cytokine activation recapitulates features of pathological inflammation in severe COVID-19. Consistently, clinical datasets show reduced CNPY2-AS1 expression in patients with fatal disease. Together, these findings reveal distinct lncRNA-mediated mechanisms regulating SARS-CoV-2 entry and identify CNPY2-AS1 as a critical integrator of redox metabolism and innate antiviral immunity. - Source: PubMed
Publication date: 2026/09/03
Khoury CarolinaAli-Nasser TahleelEliahu Yuval BenSilawi Haya DahamshyYaakov Liran BenRousseau SimonDevaux YvanLahoud-Jeries NisrineBester Assaf C - Noroviruses are a leading cause of gastroenteritis worldwide, yet host factors that restrict norovirus replication are not well understood. By mining both CRISPR activation and CRISPR knockout genome-wide screens, we identified the interferon-stimulated gene Plscr1 as a restriction factor for murine norovirus (MNV). Plscr1 inhibits the fusion of enveloped viruses with endocytic membranes, making its antiviral activity against the nonenveloped MNV surprising. Here, we demonstrate that Plscr1 is both necessary and sufficient to restrict MNV infection in vitro and contributes to the control of colonic infection in mice. Mechanistically, we determined that Plscr1 inhibits MNV entry at a post-attachment step. A single amino acid substitution in the minor capsid protein VP2 confers resistance to Plscr1. Because VP2 delivers viral RNA by puncturing endocytic membranes during calicivirus entry, these findings implicate a late entry step targeted by Plscr1. Our results expand the antiviral activity of PLSCR1 to a nonenveloped virus and identify an unexpected point of convergence between enveloped- and non-enveloped-virus entry pathways. - Source: PubMed
Publication date: 2026/09/19
Baggett Nina SPierce Linley ROrchard Robert C - Neutrophil extracellular traps (NETs) released by C-X-C motif chemokine receptor 4-high (CXCR4) neutrophils are major contributors to skin inflammation in psoriasis, yet the upstream epitranscriptomic mechanisms that regulate NETosis remain poorly defined. Here, we investigated the role of methyltransferase-like protein 7A (METTL7A) in -methyladenosine (mA)-mediated neutrophil activation and psoriasis pathogenesis. Using transcriptomic profiling of CXCR4 neutrophils from psoriasis patients, mA RNA immunoprecipitation, in vitro functional assays, and in vivo murine models of skin inflammation, along with genetic silencing and adoptive transfer experiments, we demonstrated that METTL7A was preferentially upregulated in pathogenic and aged CXCR4 neutrophils and was positively associated with disease severity. METTL7A expression also increased during human promyelocytic leukemia cells(HL-60 cell differentiation, maturation, and activation. Silencing inhibited neutrophil maturation and aging, reduced NETosis, and alleviated psoriasiform inflammation in vivo. Adoptive transfer of -deficient neutrophils further protected mice from skin inflammation. Mechanistically, METTL7A stabilized phospholipid scramblase 1 () mRNA through mA-associated regulation, thereby enhancing reactive oxygen species production and neutrophil extracellular traps (NETs) formation. These findings identify METTL7A as a novel epitranscriptomic regulator of pathogenic CXCR4 neutrophils, acting through the METTL7A-PLSCR1 axis to drive NETosis and skin inflammation, thereby providing a rationale for developing mA-targeted therapies in neutrophil-associated disorders. - Source: PubMed
Publication date: 2026/08/17
Liu WantingLiang JinkaiQuan HuiyiLiu XuanLi KangTang XinWang JiaqiGu YunfengBai YaxingXue KeLi ZhiguoSu XiaoleiDang ErleChen JiaolingWang GangShao Shuai - Aortic dissection (AD) is a life-threatening cardiovascular emergency characterized by high acute mortality. While immune dysregulation is known to drive AD pathogenesis, the specific involvement of T-cell exhaustion-related genes (TEXRGs) remains largely elusive. - Source: PubMed
Publication date: 2026/06/25
Zhang YanzhiZhao YangchaoLong XiaoqingXu Jing - Triple-negative breast cancer (TNBC) frequently acquires chemoresistance, leading to poor clinical outcomes. Phospholipid scramblase 1 (PLSCR1) has been implicated in breast cancer progression, yet its precise role and underlying mechanisms in TNBC chemoresistance remain elusive. Here, we demonstrate that PLSCR1 is significantly upregulated in chemoresistant TNBC cell lines and patient samples. Mechanistically, PLSCR1 interacts with EGFR, promoting its phosphorylation and subsequent activation of the MAPK signaling pathway, which in turn upregulates the efflux pumps P-gp and MRP1. Concurrently, PLSCR1 mRNA undergoes METTL3-mediated m6A modification, which is recognized by the m6A reader IGF2BP3, leading to enhanced mRNA stability and translational efficiency. Functional studies revealed that PLSCR1 knockdown resensitizes resistant cells to epirubicin, whereas its overexpression exacerbates resistance both in vitro and in vivo. Clinically, elevated PLSCR1 expression correlates with reduced sensitivity to neoadjuvant chemotherapy and poorer prognosis in TNBC patients. Notably, Mogroside IV-A, a specific PLSCR1 inhibitor, effectively overcomes chemoresistance by disrupting PLSCR1-mediated EGFR activation. Collectively, our findings establish PLSCR1 as a critical node integrating the METTL3/IGF2BP3 epigenetic axis with EGFR-MAPK signaling to drive TNBC chemoresistance, and highlight PLSCR1 as a promising therapeutic target for combating drug resistance in TNBC. - Source: PubMed
Publication date: 2026/05/15
Lu YaoZeng XueliangPeng ShixiongZhan YangyangLiu WenyuZhao RuiLi JingHuang QiangYe TingtingYuan ZixuanHuang Panpan