Search results for: signaling
#35045586 2022/01/19 To Up
Identification of ginsenoside metabolites in plasma related to different bioactivities of Panax notoginseng and Panax Ginseng.Although the chemical components of Panax notoginseng (PN) and Panax ginseng (PG) are similar, the bioactivities of them are different. In this study, the differential bioactivities of PN and PG were used as the research object. First, the different metabolites in the plasma after oral administration of PN and PG were analyzed by a UPLC-Q/TOF-MS-based metabolomics approach. Afterward, the metabolite-target- pathway network of PN and PG was constructed, thus the pathways related to different bioactivities were analyzed. As the results, 7 different metabolites were identified in PN group, and 10 different metabolites were identified in the PG group. In the PN group, the metabolite of N1 was related to hemostasis, N1 and N3 were related to inhibiting the nerve center, antihypertensive, and abirritation. The metabolites of N1, N3, N4, N5, and N6 were related to protecting the liver. The results showed that the metabolites of G1, G2, G3, G5, and G6 in PG group were related to anti-heart failure, and G1, G2, G6, and G9 were related to raising blood pressure. There were 13 signaling pathways related to different biological activities of PN (eight pathways) and PG (five pathways). These pathways further clarified the mechanism of action that caused the different bioactivities between PN and PG. In summary, metabolomics combined with network pharmacology could be helpful to clarify the material basis of different bioactivities between PN and PG, promoting the research on PN and PG.
Qinghai Dong, Yang An, Guangguang Du, Jia Wang, Jiayin Liu, Jun Su, Hongliu Xie, Chongyang Liang, Jihua Liu
1253 related Products with: Identification of ginsenoside metabolites in plasma related to different bioactivities of Panax notoginseng and Panax Ginseng.2 Pieces/Box100.05 mg96T
#35045414 2022/01/19 To Up
A Homozygous Missense Variant in Hedgehog Acyltransferase (HHAT) Gene Associated with 46,XY Gonadal Dysgenesis.Disorders of gonadal development represent a clinically and genetically heterogeneous group of DSD, and the etiology in many cases remains unknown, indicating that our knowledge of factors controlling sex determination is still limited.
Inas Mazen, Alaa Kamel, Kenneth McElreavey, Anu Bashamboo, Aya Elaidy, Mohamed S Abdel-Hamid
1469 related Products with: A Homozygous Missense Variant in Hedgehog Acyltransferase (HHAT) Gene Associated with 46,XY Gonadal Dysgenesis.100ug100.00 ug300 units100.00 ug1 Set1 Set1 Set50 ug100 μg100ug Lyophilized100 μg
#35045335 2022/01/16 To Up
GPR75: An exciting new target in metabolic syndrome and related disorders.The metabolic syndrome is a plethora of related disorders that are frequently associated with morbidity and mortality in addition to economic burden. While various treatment options are available, the need to understand the pathology and find new targets still remains. Recent data have suggested GPR75 as one such exciting target that has shown to a highly druggable potential. In this review, we have discussed the recent findings on GPR75 in terms of its expression and signaling and the way it could be a novel target in diseases associated with metabolic syndrome including obesity, dyslipidemia, diabetes, cardiovascular disease, and cerebrovascular disease. In addition, the opportunities and challenges related with the druggable potential of GPR75 have also been highlighted in this review.
Babar Murtaza, Faiza Asghar, Danish Patoli
2122 related Products with: GPR75: An exciting new target in metabolic syndrome and related disorders.0.1ml0.1ml (1mg/ml)2 Pieces/Box50ul (1mg/ml)0.1ml0.1ml50ul2 Pieces/Box0.1ml0.1ml0.1ml (1mg/ml)100 μg
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#35045319 2022/01/16 To Up
Extracellular traps involved in invertebrate immune mechanisms.The invertebrate immune system possesses a mechanism named extracellular traps (ETs), it has been identified that this mechanism immobilizes and kills pathogens. ETs formation induces modification of histones, chromatin decondensation, and mixes with granule molecules, releasing them into the extracellular space as a defense mechanism. In the present review, we provide an overview on the identification of triggering stimuli such as pathogens, PAMPs, DAMPs, and chemical stimuli, discuss the participation of potential signaling pathways involving MAPK, PI3K, PKC, and ERK molecules that lead to NADPH oxidase or mitochondrial ROS production, and explore the potential relationship with several proteins such as myeloperoxidase, heat sock proteins, peroxinectin, elastase, and apolipoproteins. Furthermore, we also discuss the association of ETs with other immune mechanisms that could collaborate in the elimination of pathogens.
Alicia AbigaÃl Cubillo-MartÃnez, Mohamed AlÃ Pereyra, Yonathan Garfias, Crystal Guluarte, Edgar Zenteno, JosÃ© Luis SÃ¡nchez-Salgado10mg10mg10mg5mg5mg5mg5mg10mg96 tests5mg10mg5mg
#35045313 2022/01/16 To Up
CCN2 participates in overload-induced skeletal muscle hypertrophy.The regulation of skeletal muscle growth following pro-hypertrophic stimuli requires a coordinated response by different cell types that leads to extracellular matrix (ECM) remodeling and increases in muscle cross-sectional area. Indeed, matricellular proteins serve a key role as communication vehicles that facilitate the propagation of signaling stimuli required for muscle adaptation to environmental challenges. We found that the matricellular protein cellular communication network factor 2 (CCN2), also known as connective tissue growth factor (CTGF), is induced during a time course of overload-driven skeletal muscle hypertrophy in mice. To elucidate the role of CCN2 in mediating the hypertrophic response, we utilized genetically engineered mouse models for myofiber-specific CCN2 gain- and loss-of-function and then examined their response to mechanical stimuli through muscle overload. Interestingly, myofiber-specific deletion of CCN2 blunted muscle's hypertrophic response to overload without interfering with ECM deposition. On the other hand, when in excess through transgenic CCN2 overexpression, CCN2 was efficient in promoting overload-induced aberrant ECM accumulation without affecting myofiber growth. Altogether, our genetic approaches highlighted independent ECM and myofiber stress adaptation responses, and positioned CCN2 as a central mediator of both. Mechanistically, CCN2 acts by regulating focal adhesion kinase (FAK) mediated transduction of overload-induced extracellular signals, including interleukin 6 (IL6), and their regulatory impact on global protein synthesis in skeletal muscle. Overall, our study highlights the contribution of muscle-derived extracellular matrix factor CCN2 for proper hypertrophic muscle growth.
Jennifer M Petrosino, Jacob Z Longenecker, Colin D Angel, Scott A Hinger, Colton R Martens, Federica Accornero2ug100ug100 ul96 assays96 wells200ul400 ug10 mg100 ul400 ug96T5 mg
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#35045302 // To Up
Convergent and lineage-specific genomic differences in limb regulatory elements in limbless reptile lineages.Loss of limbs evolved many times in squamate reptiles. Here we investigated the genomic basis of convergent limb loss in reptiles. We sequenced the genomes of a closely related pair of limbless-limbed gymnophthalmid lizards and performed a comparative genomic analysis including five snakes and the limbless glass lizard. Our analysis of these three independent limbless lineages revealed that signatures of shared sequence or transcription factor binding site divergence in individual limb regulatory elements are generally rare. Instead, shared divergence occurs more often at the level of signaling pathways, involving different regulatory elements associated with the same limb genes (such as Hand2 or Hox) and/or patterning mechanisms (such as Shh signaling). Interestingly, although snakes are known to have mutations in the Shh ZRS limb enhancer, this enhancer lacks relevant mutations in limbless lizards. Thus, different mechanisms could contribute to limb loss, and there are likely multiple evolutionary paths to limblessness in reptiles.
Juliana Gusson Roscito, Katrin Sameith, Bogdan Mikhailovich Kirilenko, Nikolai Hecker, Sylke Winkler, Andreas Dahl, Miguel Trefaut Rodrigues, Michael Hiller
2812 related Products with: Convergent and lineage-specific genomic differences in limb regulatory elements in limbless reptile lineages.4 Arrays/Slide4 Membranes/Box2 Pieces/Box4 Membranes/Box2 Pieces/Box4 Arrays/Slide4 Membranes/Box2 Pieces/Box4 Membranes/Box2 Pieces/Box4 Arrays/Slide4 Arrays/Slide
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#35045285 // To Up
Cx3Cr1-Cre induction leads to microglial activation and IFN-1 signaling caused by DNA damage in early postnatal brain.Cx3cr1-driven Cre recombinase (Cre) is a widely used genetic tool for enabling gene manipulation in microglia and macrophages. However, an in-depth analysis of the possible detrimental effects of Cre activity in microglia, surprisingly, remains missing. Here, we demonstrate an age-dependent sensitivity of microglia to Cx3cr1-Cre toxicity, wherein Cre induction, specifically in early postnatal microglia, is detrimental to microglial development, proliferation, and function. Tamoxifen (TAM)-induced Cre activity leads to microglial activation, type 1 interferon (IFN-1) signaling, and increased phagocytosis, causing aberrant synaptic pruning during the early postnatal period and anxious behavior at later age. The detrimental effects of Cre induction are caused by DNA-damage-induced toxicity in microglia and are limited to the early postnatal period, showing no detrimental effects in adult microglia. Thus, our study reveals an age-dependent vulnerability of microglia to Cre activity, thereby highlighting age dependency of Cre action, which could be especially applicable in the broader context of environment-responsive cell types.
Vinaya Sahasrabuddhe, Hiyaa Singhee Ghosh
1530 related Products with: Cx3Cr1-Cre induction leads to microglial activation and IFN-1 signaling caused by DNA damage in early postnatal brain.100μg100μg100 μg100ug100ug10mg100ug Lyophilized100ug Lyophilized100ug100ug10mg 100ul
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