PLP1 antibody - N-terminal region (ARP33843_P050)
- Known as:
- PLP1 (anti-) - N-terminal region (ARP33843_P050)
- Catalog number:
- arp33843_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PLP1 antibody - N-terminal region (ARP33843_P050)
Related genes to: PLP1 antibody - N-terminal region (ARP33843_P050)
- Gene:
- PLP1 NIH gene
- Name:
- proteolipid protein 1
- Previous symbol:
- SPG2, PLP
- Synonyms:
- GPM6C
- Chromosome:
- Xq22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: PLP1 antibody - N-terminal region (ARP33843_P050)
Related articles to: PLP1 antibody - N-terminal region (ARP33843_P050)
- The uncinate fasciculus (UF) is a long-range association fiber tract connecting the anterior temporal lobe with the orbitofrontal cortex and has been linked to a multitude of physiological and pathophysiological conditions such as aging, epilepsy, and the vulnerability to psychopathology posed by a history of childhood abuse (CA). Since the myelin sheath is highly enriched in lipids, changes in white matter (WM) microstructure observed via neuroimaging may reflect alterations in the myelin lipid profile. Given that the UF does not exist in rodents, its molecular properties are highly understudied. Therefore, we sought to quantify the phospholipid FA and cholesterol quantities of the human postmortem UF and evaluate any lipid-related or myelin-constituent gene/protein changes associated with age and history of CA. UF samples were analyzed from individuals with depression who died by suicide with (DS-CA) or without (DS) severe CA, and control individuals (CTRL), with an age span of 15 to 85 years. Phospholipids were separated by thin-layer chromatography; FAs and nonderivatized cholesterol were quantified by gas chromatography-flame ionization detection. The relative expression of myelin-constituent genes and proteins was measured by RT-qPCR and immunoblotting, respectively. We found no robust relationships between CA or depression and lipid measures or myelin-constituent gene/protein levels. In contrast, phospholipids showed pronounced age effects that differed by fraction, with an overall trend of monounsaturated FAs increasing and long-chain omega-6 polyunsaturated FAs decreasing with age. The expression of most myelin-constituent genes and proteins declined with age; PLP1 and MAG showed significant decreases. Therefore, changes in lipid composition and lipid-protein interactions likely contribute to age-related myelin deficits and may in part underlie age-associated cognitive decline. - Source: PubMed
Perlman KellyChen Chuck TSmith Mackenzie EKim JohnTurecki GustavoBazinet Richard PMechawar Naguib - Rhoptry proteins (ROPs) are secreted effectors that play important roles in the virulence of Toxoplasma gondii by facilitating host cell invasion and immune modulation. Although many ROPs have been predicted, their specific functions remain largely unexplored. This study investigates the roles of 11 previously uncharacterized ROPs in T. gondii biology, with a focus on their contributions to virulence. - Source: PubMed
Publication date: 2026/04/13
Song Hong-YuCao HuiHuang Shi-BoElsheikha Hany MZheng ZhiLu Xin-ShengTian XingZheng Xiao-NanZhu Xing-Quan - Coffin-Siris syndrome (CSS) is predominantly attributed to variants in ARID1B gene, however, the molecular pathways connecting ARID1B to myelination and neural development are not well elucidated. - Source: PubMed
Publication date: 2026/04/10
Yang XingkunGan ZhongzhiZhou YasiZhang MingmingWu ShuijuanHe FeiShen ZongruiMa ShunfeiSu XiXiong Fu - After invasion and replication, intracellular pathogens must egress from infected host cells. Toxoplasma gondii facilitates this process by permeabilizing host cells through induced secretion of perforin-like protein 1 (PLP1). However, the precise mechanism of host cell permeabilization remains enigmatic. Here, we identify the secretory microneme protein MIC11 as a key factor for membrane disruption. A CRISPR-based in vivo screen identifies MIC11 as the top in vivo fitness-conferring gene. Deletion of MIC11 results in severe defects in membrane rupture and egress. Scanning mutagenesis identifies functional motifs in MIC11, and mechanistic analyses support an association between MIC11 and PLP1, suggesting that MIC11 is involved in PLP1-dependent membrane disruption. Moreover, the merozoite-specific paralogue MIC22 functionally complements MIC11 deletion, suggesting a conserved mechanism of egress in the feline-restricted stages of T. gondii. Collectively, the discovery of MIC11 advances our understanding of how parasites disrupt host cells to facilitate rapid egress and successful dissemination. - Source: PubMed
Publication date: 2026/04/04
Tachibana YutaGu XueSasai MiwaKosako HidetakaTakashima EizoStandley Daron MCarruthers Vern BSoldati-Favre DominiqueYamamoto Masahiro - Obesity is a well - recognized cause of hypothalamic - pituitary hypogonadism. However, the activation patterns of whole hypothalamic neurons, the dynamic secretion of luteinizing hormone (LH) pulses and surges, and the underlying mechanisms remain unclear. We combined c-fos-based TetTag labeling, tissue clearing, and 3D imaging to map global hypothalamic neuronal activation in diet-induced obese mice. Serial blood sampling revealed how metabolic stress disrupts LH secretion dynamics-specifically its pulsatility across the estrous cycle and preovulatory surge. We further profiled transcriptional changes in activated neurons using fluorescence-activated cell sorting, Smart-seq2 sequencing, and Ingenuity Pathway Analysis. 3D imaging provides the first direct evidence that obesity globally suppresses neuronal activation in key reproductive nuclei: GFP neuron counts drop significantly in the anteroventral periventricular nucleus (525 vs. 1994), preoptic area (1821 vs. 2542), and arcuate nucleus (447 vs. 1144) versus controls. Obesity also disrupts the temporal organization of LH hormone secretion-reducing pulse frequency (4.75 ± 1.09 vs. 6.2 ± 1.4), mean and basal LH during proestrus, and abolishing the LH surge (25.0% vs. 66.7%; peak LH ∼3.0 vs. ∼7.0 ng/mL). Transcriptomic analysis identifies Sox2-mediated demyelination as the top systems-level change, evidenced by downregulation of myelin genes (e.g., Plp1, Mag) and histological confirmation of axonal loss and demyelination in these nuclei. In conclusion, these findings might uncover a previously unknown structural cause of obesity-related infertility: Sox2-mediated hypothalamic demyelination-shifting focus from functional neuroendocrine suppression to structural damage and highlighting myelin repair as a promising therapeutic strategy for restoring fertility in metabolic disorders. - Source: PubMed
Publication date: 2026/04/01
Nie YunhanGuo WenyaQiu LinLiu JialiangKuang ZheSi JiqiangZeng YuqiShen XiLiu YaliWang Li