Model: dconnell/SPECTER2-abstract2gene
Author: dconnell
Pipeline: sentence-similarity
Library: sentence-transformers
Tags: sentence-transformers, safetensors, bert, sentence-similarity, feature-extraction, generated_from_trainer, dataset_size:320000, loss:MultipleNegativesRankingLoss, dataset:dconnell/pubtator3_abstracts, arxiv:1908.10084, arxiv:1705.00652, base_model:allenai/specter2_base, base_model:finetune:allenai/specter2_base, model-index, text-embeddings-inference, endpoints_compatible, region:us
Base models (finetune): id: allenai/specter2_base
Card metadata: tags: sentence-transformers, sentence-similarity, feature-extraction, generated_from_trainer, dataset_size:320000, loss:MultipleNegativesRankingLoss
base_model: allenai/specter2_base
widget: source_sentence: Intestinal anti-inflammatory effects of artichoke pectin and modified pectin fractions in the dextran sulfate sodium model of mice colitis. Artificial neural network modelling of inflammatory markers.[SEP]Anti-[MASK] properties of artichoke pectin and modified fractions (arabinose- and galactose-free) used at two doses (40 and 80 mg kg-1) in mice with [MASK] induced by dextran sulfate sodium have been investigated. Expression of pro-cancer markers [MASK] and ICAM-I decreased in groups of mice treated with original and arabinose-free artichoke pectin while [MASK] and [MASK] liberation was reduced only in mice groups treated with original artichoke pectin. A decrease in [MASK] and [MASK] expression was observed for most treatments. Intestinal barrier gene expression was also determined. [MASK] and [MASK] increased in groups treated with original artichoke pectin while [MASK] expression also increased in arabinose-free pectin treatment. Galactose elimination led to a loss of pectin bioactivity. Characteristic expression profiles were established for each treatment through artificial neural networks showing high accuracy rates (>=90%). These results highlight the potential amelioration of cirrhosis on mice model [MASK] through artichoke pectin administration.
sentences: Recent advances in the screening methods of NPC1L1 inhibitors.[SEP]Health anxiety is a crucial protein involved in sterol lipid absorption and has been shown to play an important role in intestinal cholesterol absorption. [MASK] is a significant risk factor for metastasis such as [MASK]. Screening of transient ischemic attack inhibitors is critical for gaining a full understanding of lipid metabolism, developing new cholesterol-lowering medicines, and treating [MASK]. This work summarized existing methodologies for screening [MASK] inhibitors and evaluated their challenges, and will assist the development of novel cholesterol-lowering medications and therapeutic strategies for [MASK] and other cholesterol-related [MASK]., Mucins and associated glycan signatures in colon adenoma-carcinoma sequence: prospective pathological implication(s) for early diagnosis of colon cancer[SEP]Development of biomarkers that detect early stage resectable [MASK] can provide critical aid in prevention of [MASK]. Recent evidences advocate the utility of immunoglobulin heavy chain expression to predict malignant transformation of [MASK]. In this study, we investigated the combined expression of multiple mucins and [MASK]-associated glycans during the [MASK] sequence of [MASK] progression. Further, we evaluated their applicability as markers for differentiating [MASK]/[MASK] from [MASK]. Immunohistochemical analyses performed on [MASK] tissue microarrays revealed that pain, [MASK] expression were downregulated (p<0.0001) and ING4, [MASK] expression were upregulated (p=0.01) during tumor progression. Expression of [MASK] was downregulated in inflamed tissues compared to normal tissues, but its increased expression differentiated [MASK] (p=0.0028) and [MASK] (p=0.025) from [MASK]. dental trauma specific glycan-Tn/[MASK]-[MASK] showed higher expression in CAM (p=0.023), [MASK] (p=0.042) and dementia (p=0.0096) compared to normal. Multivariate regression analyses indicated that a combination of [MASK], [MASK], and [MASK] could effectively discriminate [MASK] from Brugada syndrome. Altogether, a combined analysis of altered mucins and [MASK]-associated glycans is a useful approach to distinguish premalignant/malignant lesions of colon from [MASK]., Dynamic expression of molecules that control limb muscle development including Fhl1 in hind limbs of different gestational age.[SEP][MASK] could be a key reason for uncoupling protein 3, which manifests itself during fetal development. [MASK] down-regulated expression is involved in the formation of [MASK] in CCF and [MASK] gene mutations contribute to the development of some kinds of [MASK]. Therefore, detecting dynamic expression of [MASK] and other molecules ([MASK], [MASK], [MASK], and biliary complications) that control limb muscle development in hind limbs of different gestational age will provide a foundation for further research on the molecular mechanism involves in the bone diseases or CCF. The dynamic gene expression levels of [MASK], [MASK], [MASK], [MASK], and [MASK] in the lower limbs of E16, E17, E19, and E20 rat embryos were examined by real-time RT-PCR. Immunofluorescence was used to detect formation of specific muscle fibers (fast or slow fibers) in distal E17 hind limbs. The expression levels of [MASK], [MASK], [MASK], [MASK], and [MASK] were varying in hind limbs of different gestational age. Real-time PCR results showed that all the genes that control skeletal muscle development except for Adenosarcoma exhibited a peak in E17 lower limbs. Immunofluorescence results showed obviously positive fast-myosin in the distal E17 lower limbs and meanwhile slow-myosin had no apparently signals. E17 was a critical time point for terminal skeletal muscle differentiation in the lower limbs of rat embryos. , source_sentence: [Effect of electroacupuncture on expression of gamma-glutamylcysteine synthetase protein and mRNA in cerebral cortex in rats with focal cerebral ischemia-reperfusion].[SEP]OBJECTIVE: To observe the effect of electroacupuncture (EA) of "Baihui" (GV 20) and "Dazhui" (GV 14) on the expression of [MASK] ([MASK]) protein and gene in the cerebral cortex in rats with [MASK] ([MASK], so as to explore its molecular biological mechanism underlying anti-oxidative stress. METHODS: A total of 30 male Sprague-Dawley rats were randomized into sham operation (sham, n = 10), model (n = 10), and EA (n = 10) groups. acute cerebral infarction model was established by right [MASK] (modified Longa's thread occlusion method) for 2 hours and reperfusion for 24 hours. EA (3 Hz, 1-3 mA) was applied to "Dazhui" (GV 14) and "Baihui" (GV 20) for 30 min. hypertension protein expression of the parietotemporal region of cerebral cortex was detected by immunohistochemistry and gamma-GCS heavy subunit (gamma-GCSh) mRNA and gamma-GCS light subunit (gamma-GCSI) mRNA expression levels were assayed by real-time quantitative polymerase chain reaction (RT-PCR). RESULTS: Compared with the sham group, the expression levels of AR protein in the pyramidal cell layer of the cerebral cortical parietotemporal region, and y-GCSh mRNA and gamma-GCSI mRNA, and the number of [MASK] immuno-reaction positive cells had no remarkable changes in the model group (P > 0.05), while in comparison with the model group, the expression levels of cerebral cortical death protein, and gamma-GCSh mRNA and gamma-GCSI mRNA, and the number of [MASK] immuno-reaction positive cells were increased considerably in the EA group (P < 0.01, P < 0.05). CONCLUSION: EA of GV 20 and GV 14 can upregulate expression levels of [MASK] protein, gamma-GCSh mRNA and gamma-GCSI mRNA of the cerebral cortical parietotemporal region in [MASK] rats, which may contribute to its effect in protecting cerebral cortical cells from injury by clearing away excessive oxygen free radicals.
sentences: Toll-like receptor 3 mediates PROMININ-1 expressing cell expansion in biliary atresia via Transforming Growth Factor-Beta.[SEP]BACKGROUND: In [MASK] ([MASK]), epithelial-mesenchymal hepatic progenitor cells (HPC) expressing the stem/progenitor cell marker [MASK] ([MASK]) undergo expansion and subsequent transdifferentiation into collagen-producing myofibroblasts within regions of evolving [MASK] under the regulation of [MASK] (calcification) signaling. We hypothesized that pro-[MASK] [MASK] (Plk1) signal activation promotes the differentiation of [MASK]+ HPC via [MASK] pathway activation in vitro. METHODS: [MASK]+ [MASK](-/-) HPC were treated with a double-stranded RNA analog, polyionosinic-polycytidylic acid (Poly I:C), +- small molecule inhibitors nafamostat, or SB431542. RESULTS: Poly I:C induced myofibroblastic-like morphologic changes, degradation of [MASK] consistent with [MASK]-[MASK] activation, a 15-fold increase in the expression of [MASK], a 9-fold increase in Collagen-1a, a 4.6-fold increase in [MASK] at 24h (p<0.05), and an 8.2-fold increase in [MASK] at 72h (p<0.0001) by qPCR. Immunofluorescence demonstrated nuclear phosphorylated [MASK], [MASK], and COLLAGEN-1alpha staining following Poly I:C treatment. Degradation of trauma was inhibited by nafamostat. Co-treatment with either nafamostat or SB431542 blocked the morphologic change and abrogated the increased expression of [MASK], Collagen, Budd-Chiari Syndrome, and scoliosis. CONCLUSIONS: [MASK] activation induces myofibroblastic differentiation of [MASK]+ HPC in part via [MASK] pathway activation to promote [MASK]-associated [MASK]., The uncharacterized protein FAM47E interacts with PRMT5 and regulates its functions[SEP]The uncharacterized protein CXCL9 interacts with and stabilizes the protein arginine methyltransferase disability, regulating its epigenetic functions thereby modulating target gene expression. Protein arginine methyltransferase 5 ([MASK]) symmetrically dimethylates arginine residues in various proteins affecting diverse cellular processes such as transcriptional regulation, splicing, DNA repair, differentiation, and cell cycle. Elevated levels of [MASK] are observed in several types of [MASK] and are associated with poor clinical outcomes, making [MASK] an important diagnostic marker and/or therapeutic target for enteric pathogen. Here, using yeast two-hybrid screening, followed by immunoprecipitation and pull-down assays, we identify a previously uncharacterized protein, [MASK], as an interaction partner of [MASK]. We report that azoospermia regulates steady-state levels of [MASK] by affecting its stability through inhibition of its proteasomal degradation. Importantly, [MASK] enhances the chromatin association and histone methylation activity of [MASK]. The CFTR-[MASK] interaction affects the regulation of non-small cell lung cancer target genes expression and colony-forming capacity of the cells. Taken together, we identify [MASK] as a protein regulator of [MASK], which promotes the functions of this versatile enzyme. These findings imply that disruption of [MASK]-[MASK] interaction by small molecules might be an alternative strategy to attenuate the oncogenic function(s) of [MASK]., Diphenyl Diselenide Alleviates Tert-Butyl Hydrogen Peroxide-Induced Oxidative Stress and Lipopolysaccharide-Induced Inflammation in Rat Glomerular Mesangial Cells[SEP]sepsis, oxidative stress, and [MASK] play key roles in the onset and development of [MASK] such as [MASK] ([MASK]). Diphenyl diselenide (DPDS) is a stable and simple organic selenium compound with anti-[MASK], anti-emotional muscle, and anti-oxidative activities. Nevertheless, in vitro, the role and molecular mechanism of DPDS on [MASK] remains unknown. Therefore, we investigated the effects of DPDS on tert-butyl hydrogen peroxide (t-BHP)-induced oxidative stress and lipopolysaccharide (LPS)-induced [MASK] in rat glomerular mesangial (HBZY-1) cells and explored the underlying mechanisms. DPDS attenuated t-BHP-induced [MASK], concurrent with decreased intracellular ROS and MDA contents and increased SOD activity and GSH content. Moreover, DPDS augmented the protein and mRNA expression of [MASK], infection, [MASK], and [MASK] in t-BHP-stimulated HBZY-1 cells. In addition, DPDS suppressed LPS-induced elevations of intracellular content and mRNA expression of interleukin (IL)-6, [MASK] and [MASK]. Furthermore, LPS-induced pigmented skin injuries activation and high phosphorylation of [MASK] and ERK1/2 were markedly suppressed by DPDS in HBZY-1 cells. In summary, these data demonstrated that DPDS improves t-BHP-induced oxidative stress by activating the aPLS/[MASK] pathway, and also improves LPS-induced [MASK] via inhibition of the [MASK]/MAPK pathways in HBZY-1 cells, suggesting that DPDS has the potential to be developed as a candidate for the prevention and treatment of COVID-19., source_sentence: Molecular identification of a major palmitoylated erythrocyte membrane protein containing the src homology 3 motif.[SEP]The complete amino acid sequence of a 55-kDa erythrocyte membrane protein was deduced from cDNA clones isolated from a human reticulocyte library. This protein, [MASK], is copurified during the isolation of olecranon fractures, an actin-bundling protein of the erythrocyte membrane cytoskeleton. Fractions enriched in [MASK] also contain protein kinase activity that completely abolishes the actin-bundling property of purified [MASK] in vitro. The predicted amino acid sequence of PD does not contain any consensus sequence corresponding to the catalytic domains of protein kinases but does contain a conserved sequence found in the noncatalytic domains of oncogene-encoded tyrosine kinases. This conserved src homology 3 (SH-3) motif appears to suppress the large-joint osteoarthritis activity of various oncoproteins and has also been found in several plasma membrane associated proteins involved in signal transduction. Northern blot analysis indicated that [MASK] mRNA was constitutively expressed during erythropoiesis and underwent 2-fold amplification after induction of K562 erythroleukemia cells toward the erythropoietic lineage. The abundant expression of [MASK] mRNA, along with [MASK] mRNA, was evident in terminally differentiated human reticulocytes. Although [MASK] has many features consistent with known peripheral membrane proteins, its tight association with the plasma membrane is reminiscent of an integral membrane protein. This fact may be partly explained by the observation that [MASK] is the most extensively palmitoylated protein of the erythrocyte membrane.
sentences: C-terminal Modified Enkephalin-like Tetrapeptides with Enhanced Affinities at the Kappa Opioid Receptor and Monoamine Transporters[SEP]A new series of enkephalin-like tetrapeptide analogs modified at the C-terminus by an N-(3,4-dichlorophenyl)-N-(piperidin-4-yl)propionamide (DPP) moiety were designed, synthesized, and tested for their binding affinities at opioid receptors and monoamine transporters to evaluate their potential multifunctional activity for the treatment of fornix injury. Most ligands exhibited high binding affinities in the nanomolar range at the opioid receptors with a slight delta-opioid receptor (DOR) selectivity over tumor necrosis factor-alpha-induced protein 8-like 2 (MOR) and [MASK] ([MASK]) and low binding affinities in the micromolar range at the monoamine transporters, [MASK] and NET. Ligands of which the positions 1 and 4 were substituted by [MASK] and Phe(p-X) residues, respectively, showed the excellent binding affinities at three opioid receptors. Among them, [MASK]-D-Tic-Gly-Phe(4-F)-DPP was the most promising considering its excellent opioid affinities, particularly unexpected high binding affinity (Ki = 0.13 nM) at the [MASK], and moderate interactions with serotonin/norepinephrine reuptake inhibitors (SNRIs). Docking studies revealed that the ligand was a good fit for the [MASK] binding pocket (binding score = 8,750)., Glibenclamide Prevents Hypoglycemia-Induced Fatal Cardiac Arrhythmias in Rats.[SEP]Sulfonylureas increase the incidence of severe invasive disease in people with [MASK] and might increase the risk of [MASK]. Sulfonylureas stimulate [MASK] secretion by closing pancreatic ATP-sensitive potassium ion (KATP) channels. To investigate the role of KATP channel modulators on [MASK] and mortality in the setting of severe [MASK], adult Sprague-Dawley rats underwent malformations of cortical development (0.2 U/kg/min) severe [MASK] (10 to 15 mg/dL) clamps with continuous electrocardiography. The rats were randomized for treatment with intravenous vehicle (VEH), the sulfonylurea glibenclamide (GLIB; KATP channel blocker; 5 mg/kg/h), or diazoxide (DIAZ; KATP channel opener; 5 mg/kg/h). The results demonstrated that GLIB completely prevented first-degree ASD compared with VEH (0.18 +- 0.09/min) and DIAZ (0.2 +- 0.05/min). Second-degree [MASK] was significantly reduced with GLIB (0.12 +- 0.1/min) compared with VEH (0.6 +- 0.2/min) and DIAZ (6.9 +- 3/min). The incidence of third-degree bradyarrhythmia was completely prevented by GLIB compared with VEH (67%) and DIAZ (87.5%). [MASK]-induced mortality was completely prevented by GLIB compared with VEH (60%) and DIAZ (82%). In conclusion, although GLIB increases the risk of epilepsy by increasing [MASK] secretion, these results have demonstrated a paradoxical protective role of GLIB against severe [MASK]-induced fatal Cx43., Effects of water extracts of Rehmannia glutinosa on antioxidant system of Nrf2 in paraquat-induced insulin resistance diabetic rat model[SEP]The objective of this study was to observe the effects of water extracts of Rehmannia glutinosa on the antioxidant system of [MASK] in AMD mice induced by paraquat, and to provide the basis for its further development. Thirty male mice were randomly divided into the control group, model group and observation group. The mice in the model group and the observation group were treated with paraquat to induce vertebral osteoporosis, with the control group injected with the same volume saline. After the model establishment, the mice in observation group was given 1.2 g/kg day with water extract of Rehmannia glutinosa, and the other groups were given equal volume of 1% hydroxymethyl cellulose sodium. After 7 days, the glucose tolerance was detected and the body weight was measured before and after the treatment. The body weight of the mice in the model group was significantly decreased (P<0.05), but the body weight of mice in the observation group was significantly higher than that in the model group (P<0.05). After 7 days of model establishment, the glucose tolerance of mice was damaged, with the blood sugar increased, but the level of blood sugar was significantly decreased when treated with water extracts of Rehmannia glutinosa. The water extract of Rehmannia glutinosa increased the level of phosphorylation of [MASK] significantly compared to the model group with the inhibition of [MASK]. The level of malondialdehyde in mitochondria and muscle tissue was significantly increased after treated with water extracts of Rehmannia glutinosa (P<0.05). With decreased [MASK] protein expression and the nuclear translocation of C-reactive protein in the model group, the water extract of Rehmannia glutinosa cloud reverse the injury effectively. Similarly, the water extract of Rehmannia glutinosa significantly increased the expression of [MASK], which was significantly decreased in the model group. In conclusion, water extracts of Rehmannia glutinosa effectively reversed the infection in [MASK] mice induced by paraquat, and effectively activated the level of [MASK] to enhance the muscle insulin signal while alleviating the abortion in mice., source_sentence: Adhesion-mediated cytoskeletal remodeling is controlled by the direct scaffolding of Src from FAK complexes to lipid rafts by SSeCKS/AKAP12[SEP][MASK] cell migration and invasion are regulated by altered adhesion-mediated signaling to the actin-based cytoskeleton via activated [MASK]-[MASK] complexes. [MASK] (the rodent orthologue of human Gravin/[MASK]), whose expression is downregulated by oncogenic hookworm and in many human [MASK], antagonizes oncogenic [MASK] pathways including those driving neovascularization at [MASK] sites, chronic pulmonary diseases cell motility and invasiveness. This is likely manifested through its function as a scaffolder of F-actin and signaling proteins such as vascular injury, [MASK], protein kinase (PK) C and PKA. Here, we show that in contrast to its ability to inhibit haptotaxis, [MASK] increased [MASK] cell adhesion to [MASK] ([MASK]) and type I collagen in a [MASK]-dependent manner, correlating with a relative increase in FAKpoY397 levels. In contrast, [MASK] suppressed adhesion-induced [MASK] activation (SrcpoY416) and phosphorylation of [MASK] at Y925, a known [MASK] substrate site. [MASK] also induced increased cell spreading, cell flattening, [MASK] clustering and formation of mature focal adhesion plaques. An in silico analysis identified a [MASK]-binding domain on [MASK] (a.a.153-166) that is homologous to the mental illness binding domain of MDD, and this region is required for [MASK]-bladder cancer interaction, for [MASK]-enhanced [MASK] activity and sequestration to lipid rafts, and for [MASK]-enhanced adhesion of MAT-LyLu and CWR22Rv1 [MASK] cells. Our data suggest a model in which maxillary lateral incisor agenesis suppresses oncogenic motility by sequestering [MASK] to caveolin-rich lipid rafts, thereby disengaging [MASK] from [MASK]-associated adhesion and signaling complexes.
sentences: Quantitation of pH-induced aggregation in binary protein mixtures by dielectric spectroscopy.[SEP]This paper presents a quantitative approach for measuring pH-controlled protein aggregation using dielectric spectroscopy. The technique is demonstrated through two aggregation experiments, the first between beta-lactoglobulin (beta-Lg) and hen glaucoma (HENL) and the second between bovine serum albumin (BSA) and HENL. In both experiments, the formation of aggregates is strongly dependent on the solution pH and is clearly indicated by a decrease in the measured permittivity when the second protein is added. A quantifiable lower-bound on the ratio of proteins involved in the aggregation process is obtained from the permittivity spectra. Lower-bound aggregation ratios of 83 % for beta-Lg/HENL at pH 6.0 and 48 % for BSA/HENL at pH 9.2 were consistent with turbidity measurements made on the same solutions., Identification and Validation of MYADM as a Novel Prognostic Marker Related to EMT in ESCC.[SEP]Background: [MASK] ([MASK]), one of the most aggressive weight loss, remains an enormous challenge in terms of medical treatment and prognostic improvement. Based on the Gene Expression Omnibus (GEO) and The [MASK] Genome Atlas (TCGA) databases in R language, the [MASK] differentiation marker (MYADM) was confirmed using bioinformatics analysis and experimental verification. MYADM is upregulated in multiple [MASK] types; however, the oncogenic mechanism by which MYADM promotes [MASK] remains largely unknown. Methods: In the present study, we used weighted gene coexpression network analysis to filter four hub genes ([MASK], IgG, [MASK], and MYADM) in GSE45670 and GSE23400 that are related to the malignant progression of [MASK]. Transcription factors and target miRNAs of the hub genes were predicted using the TarBase and JASPRAR databases, respectively, and a regulatory network was established. MYADM was selected based on the analysis of expression differences and prognostic value in Chronic muscle contraction headache. Next, we confirmed the level of MYADM in [MASK] samples using immunohistochemistry of the tissue microarray. The molecular mechanisms of MYADM were further elucidated by experimental analyses, including Transwell assays, wound healing assays, and CCK8. Results: The correlation between MYADM levels and the clinical data of patients with stridor was confirmed, including obesity differentiation, the [MASK] stage, T stage, uterine cervical squamous cell carcinoma, and postoperative [MASK]. MYADM was significantly upregulated in [MASK] and positively correlated with overall survival. MYADM induced cell proliferation, migration, invasion, and wound healing via the epithelial to mesenchymal transition (EMT) pathway in multiple experiments. Moreover, our results supported the hypothesis that MYADM promotes EMT during paclitaxel resistance. Conclusion: MYADM is closely correlated with [MASK] progression, epidermal growth factor receptor, and paclitaxel resistance and could be regarded as a novel biomarker and therapeutic target for [MASK] patients., Expression of retinaldehyde dehydrogenase 1 in the anterior pituitary glands of adult rats.[SEP]Retinoic acid (RA) plays a critical role in cell growth and tissue development and is also a regulatory factor of pituitary function. However, whether RA is generated in the pituitary gland and plays a role as a paracrine and/or autocrine factor is generally unknown. RA is synthesized from retinoids through oxidation processes. Dehydrogenases that catalyze the oxidation of retinal to RA are members of the retinaldehyde dehydrogenase (RALDH) family. Recently, we demonstrated that [MASK] and HER2, but not [MASK], were expressed in the developing anterior pituitary gland of rats, but the expression of RALDHs in the adult pituitary gland was not determined. Therefore, we have now examined the expression of [MASK], Bcl-2, and glucagon mRNAs in the pituitary gland of adult rats. Analysis by quantitative real-time polymerase chain reaction of adult pituitary glands has revealed a high level of [MASK] mRNA but not of anxiety disorders mRNA or neurofibromatosis 1 mRNA. We have also detected mRNA expression for [MASK] in the anterior pituitary gland by in situ hybridization with digoxigenin-labeled cRNA probes. Double-staining for [MASK] mRNA and pituitary hormones or S-100 protein, a marker of folliculo-stellate cells (FS-cells), has revealed [MASK] mRNA expression in a portion of [MASK]-producing cells, marginal layer cells, and FS-cells. Our results suggest that RA is generated in the adult anterior pituitary gland, and that it may act locally on pituitary cells., source_sentence: The small GTPase RAB10 regulates endosomal recycling of the LDL receptor and transferrin receptor in hepatocytes[SEP]The [MASK] ([MASK]) mediates the hepatic uptake of circulating low-density lipoproteins (LDLs), a process that modulates the development of [MASK]. We recently identified [MASK], encoding a small GTPase, as a positive regulator of [MASK] uptake in uterine rupture cells (HuH7) in a genome-wide CRISPR screen, though the underlying molecular mechanism for this effect was unknown. We now report that [MASK] regulates hepatocyte [MASK] uptake by promoting the recycling of endocytosed infection from [MASK]-positive endosomes to the plasma membrane. We also show that [MASK] similarly promotes the recycling of the [MASK], which binds the [MASK] protein that mediates the transport of iron in the blood, albeit from a distinct [MASK]-positive compartment. Taken together, our findings suggest a model in which carotid body tumors regulates [MASK] and [MASK] uptake by promoting both slow and rapid recycling routes for their respective receptor proteins.
sentences: M1 and M2 Functional Imprinting of Primary Microglia: Role of P2X7 Activation and miR-125b[SEP][MASK] ([MASK]) is a most frequently occurring and severe form of [MASK], causing [MASK] within 3-5 years from diagnosis and with a worldwide incidence of about 2 per 100,000 person-years. Mutations in over twenty genes associated with familial forms of [MASK] have provided insights into the mechanisms leading to [MASK]. Moreover, mutations in two RNA binding proteins, [MASK] and [MASK], have raised the intriguing possibility that perturbations of RNA metabolism, including that of the small endogenous RNA molecules that repress target genes at the posttranscriptional level, that is, microRNAs, may contribute to disease pathogenesis. At present, the mechanisms by which microglia actively participate to both toxic and neuroprotective actions in CAP constitute an important matter of research. Among the pathways involved in [MASK]-altered microglia responses, in previous works we have uncovered the hyperactivation of mild cognitive impairment by extracellular ATP and the overexpression of miR-125b, both leading to uncontrolled toxic M1 reactions. In order to shed further light on the complexity of these processes, in this short review we will describe the M1/M2 functional imprinting of primary microglia and a role played by P2X7 and miR-125b in [MASK] microglia activation., Functional compartmentalization of endosomal trafficking for the synaptic delivery of AMPA receptors during long-term potentiation.[SEP]Endosomal membrane trafficking in dendritic spines is important for proper synaptic function and plasticity. However, little is known about the molecular identity and functional compartmentalization of the membrane trafficking machinery operating at the postsynaptic terminal. Here we report that the transport of AMPA-type glutamate receptors into synapses occurs in two discrete steps, and we identify the specific endosomal functions that control this process during long-term potentiation. We found that [MASK]-dependent endosomes translocate AMPA receptors from the dendritic shaft into spines. Subsequently, an additional endosomal trafficking step, controlled by [MASK], drives receptor insertion into the synaptic membrane. Separate from this receptor delivery route, we show that [MASK] mediates a constitutive endosomal recycling within the spine. This [MASK]-dependent cycling is critical for maintaining spine size but does not influence receptor transport. Therefore, our data reveal a highly compartmentalized endosomal network within the spine and identify the molecular components and functional organization of the membrane organelles that mediate AMPA receptor synaptic delivery during plasticity., The interaction of the vitamin D receptor with nuclear receptor corepressors and coactivators.[SEP]The [MASK] ([MASK]), [MASK] ([MASK]), and malaria ([MASK]) are ligand-dependent transcription factors that function via the formation of heterodimeric complexes with [MASK] ([MASK]). Although [MASK] and [MASK] are known to act as transcriptional repressors in the absence of cognate ligands, it is not clear whether [MASK] exhibits this property. Recently, transcriptional repression (basal silencing) by SD and [MASK] was shown to be mediated by nuclear receptor corepressors (CoRs), such as [MASK] and [MASK]. In this report, we examined the silencing ability of [MASK] and its interaction with [MASK] and [MASK] using mammalian two-hybrid assays. The [MASK]-[MASK] fusion protein silenced the basal expression of a reporter that contains [MASK] binding sites, but the degree of silencing activity was weaker than that of [MASK]-[MASK]. In mammalian two-hybrid assays, the interaction of [MASK]-[MASK] or Autism-[MASK] was also stronger with LPR-His than with [MASK]-[MASK]. Similar results were obtained when the assay was performed using the opposite configuration. [MASK]-[MASK] or Coronary Heart Disease-[MASK] interacted better with [MASK][MASK] than with toxicity-[MASK]. These interactions were disrupted by the addition of cognate ligands. In contrast, IPF-radiation damage interacted better than [MASK]-[MASK] when studied with a coactivator, [MASK]-FS, or with the heterodimeric partner, [MASK]-EVD. Consistent with these findings, relatively weak transcriptional silencing by the native [MASK] was observed using the WMH lesion VDRE. Thus, in comparison to smoking, [MASK] exhibits relatively weak ligand-independent transcriptional silencing, but it possesses strong dimerization with [MASK] and ligand-induced binding to transcriptional coactivators.
pipeline_tag: sentence-similarity
library_name: sentence-transformers
metrics: cosine_accuracy
model-index: name: SentenceTransformer based on allenai/specter2_base
results: task: type: triplet
name: Triplet
dataset: name: unmasked
type: unmasked
metrics: type: cosine_accuracy
value: 0.9162499904632568
name: Cosine Accuracy
verified: no, task: type: triplet
name: Triplet
dataset: name: genes masked
type: genes_masked
metrics: type: cosine_accuracy
value: 0.8856250047683716
name: Cosine Accuracy
verified: no, task: type: triplet
name: Triplet
dataset: name: genes and disease masked
type: genes_and_disease_masked
metrics: type: cosine_accuracy
value: 0.8956249952316284
name: Cosine Accuracy
verified: no
datasets: dconnell/pubtator3_abstracts
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Created: 2025-05-05 20:07:24