LPPR2 Blocking Peptide
- Known as:
- LPPR2 Blocking Peptide
- Catalog number:
- 33r-6943
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- LPPR2 Blocking Peptide
Related genes to: LPPR2 Blocking Peptide
- Gene:
- PLPPR2 NIH gene
- Name:
- phospholipid phosphatase related 2
- Previous symbol:
- -
- Synonyms:
- LPPR2, PRG-4
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2015-10-14
- Date modifiied:
- 2015-10-14
Related products to: LPPR2 Blocking Peptide
Related articles to: LPPR2 Blocking Peptide
- Myocardial infarction(MI), a severe and often fatal cardiovascular condition, strongly contributes to global mortality and morbidity. Lipids are critical underlying factors in cardiovascular disease. They influence inflammatory responses and modulate leukocyte, vascular cell and cardiac cell functions, affecting the vasculature and heart. We aimed to identify novel biomarkers and therapeutic targets for MI that are linked to lipid metabolism. - Source: PubMed
Publication date: 2025/07/09
Wang QiangWu XianYu Bo - Neuroinflammation has been implicated as a pathological contributor to several neurodegenerative disorders. Increasing evidence suggests that paracetamol (PCM, acetaminophen) has unappreciated anti-neuroinflammatory properties. However, PCM possesses hepatotoxicity in higher dosages, which are needed for achieving therapeutic concentrations in the brain. To lessen this effect and improve drug efficacy, PCM was in this study converted into an L-type amino acid transporter 1 (LAT1)-utilizing derivative and tested whether this LAT1-mediated delivery approach could enhance the relief of neuroinflammation, using both in vitro and in vivo lipopolysaccharide (LPS)-stimulated models. The gained results confirmed the derivative's improved transport into mouse primary astrocytes, immortalized microglia (BV2), and human immortalized microglia (SV40) via LAT1. In the LPS-stimulated BV2 model, the derivative effectively reduced the prostaglandin E (PGE) level by 57% compared to the LPS treatment. Moreover, a more profound reduction of brain PGE production was confirmed in the LPS-stimulated mouse model. Finally, the global proteome of the whole mouse brain revealed that the derivative was able to reverse the altered expression of several inflammatory biomarkers, including ras-related C3 botulinum toxin substrate 1 (Rac1), cytochrome c oxidase subunit 2 (COX2), phospholipid phosphatase-related protein type 2 (Plppr2), ubiquitin-conjugating enzyme E2 variant 1 (Ube2v1) and A-kinase anchor protein 1, mitochondrial (Akap1). - Source: PubMed
Publication date: 2025/02/20
Králová AdélaMontaser Ahmed BTampio JanneAdla Santosh KumarJalkanen AaroRysä JaanaHuttunen Kristiina M - Lysophosphatidic acid (LPA) is a bioactive phospholipid that participates in critical processes in neural development and adult brain function and is implicated in various pathophysiological conditions. Along with its six well-characterized receptors, atypical regulators of LPA signaling have also been suggested, including phospholipid phosphatase-related proteins (PLPPRs). PLPPRs have been mostly studied in the developing brain where they control LPA-dependent axon guidance, cortical network hyperexcitability, and glutamatergic neurotransmission. PLPPR4 and PLPPR3 represent two closely related proteins reported to localize predominantly in dendrites and axons, respectively, and differ in their developmental expression patterns. Herein, we have revised the expression patterns of PLPPRs in the cerebellum, dorsal and ventral hippocampus, prefrontal cortex (PFC), nucleus accumbens, and striatum during development and in the adult using quantitative PCR. Expression patterns of Plppr2,4 and 5 were consistent with previous studies, whereas Plppr3 and Plppr1 exhibited a unique expression profile in nucleus accumbens (NAc) and striatum in later developmental and adult stages, which we verified at the protein level for PLPPR3. To investigate neuron type-specific expression at the single cell level, we developed a bioinformatic tool to analyze recent single-cell RNA-sequencing data in the cerebral cortex and hippocampus of adult mice. Our analysis revealed a widespread but also selective adult neuron-type expression with higher expression levels of Plppr3, Plppr1, and Plppr5 in GABAergic and Plppr4 and Plppr2 in glutamatergic neurons. PLPPR4 has been identified as a post-synaptic modulator of LPA levels in glutamatergic synapses operating via an uptake mechanism, to control LPA-dependent cortical network hyperexcitability. Using subcellular fractionation experiments, we found that both PLPPR4 and PLPPR3 are co-expressed in adult synaptosomal membranes. Furthermore, flow cytometry experiments in HEK293 cells showed comparable LPA uptake by PLPPR4 and PLPPR3, whereas PLPRR3, but not PLPPR4, induced also uptake of monoacylglycerol, the dephosphorylation product of LPA. We propose that synaptic LPA may be subject to both pre-synaptic and post-synaptic mechanisms of regulation by PLPPRs in addition to LPARs in developing and adult synapses. - Source: PubMed
Publication date: 2024/07/12
Polyzou AlexandraFuchs JoachimKroon CristinaKotoula AndronikiDelis FoteiniTurko PaulAntoniou KaterinaEickholt BrittaLeondaritis George - Image-based screening improves the detection of early-stage lung adenocarcinoma (LUAD)but also highlights the issue of high false-positive diagnoses, which puts patients at a risk of unnecessary over-treatment. Therefore, more precise discrimination criteria are required to ensure that patients with early-stage LUAD receive appropriate treatments. - Source: PubMed
Publication date: 2023/11/23
Wang YibeiMiao ZiweiQin XiaoxueYang YiWu SiMiao QiLi BeibeiZhang MingyuWu PengfeiHan YunLi Bo - LPP2 is one of three enzymes in the lipid phosphate phosphatase family (LPP1-3) that dephosphorylate extracellular and intracellular bioactive lipid phosphates and pyrophosphates. LPP2 increases cell growth and LPP2 expression is elevated in a variety of malignancies, implying that LPP2 is a pro-tumorigenic factor. LPP2 expression in human breast tumors and normal breast tissue was measured by qPCR. To understand the role of LPP2, we knocked out its expression in multiple cell lines using CRISPR/Cas9. Cell proliferation and migration were compared between wild type and LPP2 knockout cells. Cell cycle was measured by flow cytometry, and cell cycle proteins were determined by western blotting. Effects of LPP2 on tumor growth were investigated using syngeneic and xenograft mouse breast cancer models. LPP2 mRNA levels were higher in ER/PR positive, ER/HER2 positive, and triple negative human breast tumors, relative to normal breast tissue. Higher levels of LPP2 in breast tumors, hepatocellular carcinoma, pancreatic adenocarcinoma, and melanomas were prognostic of poorer survival. LPP2 mRNA expression is also increased in Hs-578T, MDA-MB-231, MCF7 and MDA-MB-468 breast cancer cell lines, relative to non-malignant Hs-578Bst, MCF10A and MCF-12A cells. LPP2 knockout in breast cancer cells decreased cell growth by inhibiting G1/S transition, whereas, increasing LPP2 levels in Hs-578Bst and MCF10A cells promoted proliferation. The effects of LPP2 on cell cycle were associated with changes in cyclin A2, cyclin B1, and cell cycle inhibitors, p27 or p21. The level of c-Myc was downregulated by knocking out LPP2, and it was partly restored by re-expressing LPP2. The positive correlation between the expression of LPP2 and c-Myc exists in multiple cancer cell lines including breast, lung, upper aerodigestive tract and urinary tract cancer. LPP2 knockout in MDA-MB-231 or 4T1 cells suppressed tumor formation in mouse breast cancer models, and decreased the expression of Ki67 and c-Myc of the cancer cells. Targeting LPP2 could provide a new strategy for decreasing c-Myc expression and tumor growth. - Source: PubMed
Publication date: 2022/07/18
Tang XiaoyunCromwell Christopher RLiu RongzongGodbout RoselineHubbard Basil PMcMullen Todd P WBrindley David N