PGRPS antibody Polyclonal Antibodies Primary antibodies
- Known as:
- PGRPS (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100615
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- PGRPS antibody Polyclonal Antibodies Primary antibodies
Related genes to: PGRPS antibody Polyclonal Antibodies Primary antibodies
- Gene:
- PGLYRP1 NIH gene
- Name:
- peptidoglycan recognition protein 1
- Previous symbol:
- TNFSF3L, PGLYRP
- Synonyms:
- TAG7, PGRP, PGRP-S, PGRPS
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-15
- Date modifiied:
- 2015-07-22
Related products to: PGRPS antibody Polyclonal Antibodies Primary antibodies
Related articles to: PGRPS antibody Polyclonal Antibodies Primary antibodies
- Bovine mastitis, caused by bacterial infection of the mammary gland, leads to significant economic losses for the dairy industry because of decreased milk quality and yield. Mastitis is typically treated with conventional antibiotics (ABX) that clear bacteria, but do not address the milk loss associated with infection. Milk from cows being treated with ABX must be discarded leading to acute milk loss, and ABX do not heal milk-producing tissues that are damaged because of infection, leading to a permanent reduction in milk production when compared to pre-mastitis levels. The bovine mammosphere-derived epithelial cell (MDEC) secretome, consisting of all bioactive factors secreted by the cells, contains molecules that directly and indirectly promote tissue repair. This current study shows that the MDEC secretome also inhibits the growth of mastitis-causing bacteria in planktonic and biofilm assays. Secretome analysis by heat treatment, size fractionization, and extracellular vesicle isolation suggested that soluble proteins of different sizes, or in complexes, drive the anti-bacterial effects. We identified the antimicrobial protein peptidoglycan recognition protein 1 (PGLYRP1) in MDECs and detected it in the secretome. As knock down of PGLYRP1 expression in MDECs was unsuccessful using RNA interference and CRISPR-Cas9 gene editing, a direct link between the antimicrobial activity of the secretome and this protein could not be confirmed. The newly identified antimicrobial activity of the bovine MDEC secretome supplements its tissue reparative features, poising it as a potential adjunct or alternative therapy for bovine mastitis that may reduce acute milk loss and improve long term milk production. - Source: PubMed
Publication date: 2026/03/31
Harman Rebecca MDanev NikolaOxford Kelly AOliveira LeaneHuntimer LucasVan de Walle Gerlinde R - Peptidoglycan recognition proteins (PGRPs) constitute an evolutionarily conserved family of pattern recognition molecules that detect bacterial peptidoglycan. While their antimicrobial functions have been well characterized in peripheral immunity, recent discoveries have unveiled critical roles for PGRPs in central nervous system inflammation and behavior. Among the four mammalian PGRP family members, PGLYRP1 exhibits unique expression in brain microglia and demonstrates potent pro-inflammatory properties in neurological contexts. Recently, PGLYRP1 has been shown to function as a key amplifier of neuroinflammation through a novel TREM1-Syk-Erk1/2-Stat3 signaling axis, establishing a positive feedback loop with TNF-α that perpetuates microglial activation. This review synthesizes current understanding of PGRP biology in the nervous system, with particular emphasis on molecular mechanisms of PGLYRP1, cellular sources, and behavioral consequences. We examine the structural basis of peptidoglycan recognition, cell-type-specific expression patterns, signaling pathways, and integration with other innate immune systems. Furthermore, we explore emerging connections between gut microbiome-derived peptidoglycan, blood-brain barrier penetration, and neuropsychiatric disorders. Critical knowledge gaps remain regarding physiological versus pathological roles of PGLYRP1, therapeutic targeting strategies, and translational potential. Understanding PGLYRP1-mediated neuroinflammation provides novel mechanistic insights into microbiome-brain communication and offers promising therapeutic avenues for neuroinflammatory and neurodegenerative diseases. - Source: PubMed
Publication date: 2026/03/18
Suk KyounghoLee Won-Ha - Endothelial cells (ECs) are key structural and functional components of the blood-brain barrier (BBB). Mouse models are frequently used to study EC biology within the BBB, yet the extent to which human and mouse BBB ECs share conserved transcriptomic features remains unclear. Here, we systematically compare transcriptomic profiles of BBB capillary ECs from adult mice and humans. - Source: PubMed
Publication date: 2026/03/12
Miao YuyangWang JianhaoLi WeihanMäe Maarja AndaloussiJeansson MarieMuhl LarsHe Liqun - The maintenance of immune homeostasis is critical for tissue health and longevity, yet the regulatory mechanisms linking immune modulation to aging remain poorly understood. Here we found that the transcription factor cAMP response element-binding protein (CREB), activated by JNK signaling in aging guts, transcriptionally suppresses peptidoglycan recognition protein SC2(PGRP-SC2)-a homolog of anti-inflammatory PGLYRP1-4 with amidase activity. 16S rRNA sequencing revealed that CREB modulates not only microbial load but also microbiota composition. Elevated CREB activity decreased the Firmicutes/Bacteroidetes (F/B) ratio-a hallmark of age-associated dysbiosis in animals. Genetic enhancement of PGRP-SC2 rescues age-related gut hyperplasia, microbiota imbalance, and lifespan shortening induced by overactivation of CREB or its coactivator CRTC. Notably, CREB's regulation of PGRP-SC2 operates independently of canonical immune pathways such as Imd/Relish, revealing a previously unrecognized layer of immune modulation. Our findings establish CREB as a central player in age-associated immune dysregulation and propose targeting the CREB-PGRP-SC2 axis as a potential therapeutic strategy for mitigating gut aging and its systemic consequences. - Source: PubMed
Publication date: 2026/02/24
Wang SaifeiQi BohanMa PengZhang YaoYin YoujieChen ShuxinDeng Hansong - Excessive neutrophil activation and neutrophil extracellular trap (NET) release drive systemic inflammation and organ injury in sepsis, yet the upstream regulatory pathways remain incompletely defined. Here, we identify epidermal growth factor receptor (EGFR) as a critical neutrophil-intrinsic regulator of NETosis. EGFR expression was markedly elevated in neutrophils from patients with sepsis and correlated with disease severity. Neutrophil-specific EGFR deletion in mice improved survival after polymicrobial sepsis by reducing cytokine storm, tissue injury, and NET formation. Mechanistically, EGFR associated with CCAAT/enhancer-binding protein beta (CEBPβ) and recruited Mitogen-activated protein kinase 14 (MAPK14) to phosphorylate CEBPβ, promoting its nuclear localization and transcriptional activation of peptidoglycan recognition protein 1 (PGLYRP1). Elevated PGLYRP1, in turn, amplified NETs release via autocrine engagement of triggering receptor expressed on myeloid cell-1 (TREM-1), establishing a feed-forward inflammatory loop. Administration of recombinant PGLYRP1 or forced CEBPβ overexpression reversed the protection conferred by EGFR deficiency, confirming the centrality of this axis. These findings define an unrecognized EGFR-MAPK14-CEBPβ-PGLYRP1-TREM1 circuit that links receptor signaling to pathological NETosis and highlight a promising therapeutic target to attenuate neutrophil-driven immunopathology in sepsis. - Source: PubMed
Publication date: 2026/01/15
Liu XiaoleiLu YueGuo YuanboHuang GuorongLi JiahuiLin JingranLi ZhijieZhang LiangqingZhong HanhuiZhang YiwenTang Jing