Log in

Relevant bibliographies by topics / Scge30 / Journal articles

Journal articles on the topic 'Scge30'

To see the other types of publications on this topic, follow the link: Scge30.

Author: Grafiati

Published: 26 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Scge30.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Lukashenko, G. M., V. R. Sidorko, and Yu I. Buyanov. "Thermodynamic properties of the scandium germanides ScGe2 and ScGe." Soviet Powder Metallurgy and Metal Ceramics 29, no. 7 (July 1990): 568–70. http://dx.doi.org/10.1007/bf00796073.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Tararuk, Tatsiana, Nina Östman, Wenrui Li, Benny Björkblom, Artur Padzik, Justyna Zdrojewska, Vesa Hongisto, et al. "JNK1 phosphorylation of SCG10 determines microtubule dynamics and axodendritic length." Journal of Cell Biology 173, no. 2 (April 17, 2006): 265–77. http://dx.doi.org/10.1083/jcb.200511055.

Full text

Abstract:

c-Jun NH2-terminal kinases (JNKs) are essential during brain development, when they regulate morphogenic changes involving cell movement and migration. In the adult, JNK determines neuronal cytoarchitecture. To help uncover the molecular effectors for JNKs in these events, we affinity purified JNK-interacting proteins from brain. This revealed that the stathmin family microtubule-destabilizing proteins SCG10, SCLIP, RB3, and RB3′ interact tightly with JNK. Furthermore, SCG10 is also phosphorylated by JNK in vivo on sites that regulate its microtubule depolymerizing activity, serines 62 and 73. SCG10-S73 phosphorylation is significantly decreased in JNK1−/− cortex, indicating that JNK1 phosphorylates SCG10 in developing forebrain. JNK phosphorylation of SCG10 determines axodendritic length in cerebrocortical cultures, and JNK site–phosphorylated SCG10 colocalizes with active JNK in embryonic brain regions undergoing neurite elongation and migration. We demonstrate that inhibition of cytoplasmic JNK and expression of SCG10-62A/73A both inhibited fluorescent tubulin recovery after photobleaching. These data suggest that JNK1 is responsible for regulation of SCG10 depolymerizing activity and neurite elongation during brain development.

APA, Harvard, Vancouver, ISO, and other styles

3

Pampfer, S., W. Fan, UK Schubart, and JW Pollard. "Differential mRNA expression of the phosphoprotein p19/SCG10 gene family in mouse preimplantation embryos, uterus, and placenta." Reproduction, Fertility and Development 4, no. 2 (1992): 205. http://dx.doi.org/10.1071/rd9920205.

Full text

Abstract:

The p19/SCG10 gene family encodes two structurally related cellular proteins that are implicated in signal transduction during differentiation of mammalian cells. Previous evidence suggests that both genes are expressed in a stage-specific manner but that expression of p19 is widespread, whereas that of SCG10 is restricted to developing neurons. To determine at which developmental stage these two genes are first expressed, we have probed for mRNA transcripts in preimplantation embryos and the utero-placental unit of the mouse. As determined by polymerase chain reaction (PCR) to amplify reverse-transcribed RNA, expression of both genes was detected in preimplantation embryos, although the temporal pattern was distinct. p19 mRNA appeared transiently in 2-cell embryos, was undetectable in morulae and early blastocysts and reappeared in expanded blastocysts. In contrast, embryonic expression of SCG10 mRNA commenced in morulae and was maintained through to the blastocyst stage. Interestingly, only SCG10 expression could be detected in blastocysts derived from cultures of 2-cell embryos. During the post-implantation period, SCG10 transcripts were only detected in the uterus and placenta by reverse transcriptase-PCR, whereas p19 mRNA could be detected by Northern blotting and showed stage-specific expression in both tissues. The data confirm that, at later developmental stages, expression of p19 is widespread while that of SCG10 is more restricted. The expression of both genes in preimplantation embryos suggests distinct but possibly overlapping roles for p19 and SCG10 in early mammalian development.

APA, Harvard, Vancouver, ISO, and other styles

4

Zhang, Han, Xinghua Lu, Binfeng Lu, and Lujia Chen. "scGEM: Unveiling the Nested Tree-Structured Gene Co-Expressing Modules in Single Cell Transcriptome Data." Cancers 15, no. 17 (August 26, 2023): 4277. http://dx.doi.org/10.3390/cancers15174277.

Full text

Abstract:

Background: Single-cell transcriptome analysis has fundamentally changed biological research by allowing higher-resolution computational analysis of individual cells and subsets of cell types. However, few methods have met the need to recognize and quantify the underlying cellular programs that determine the specialization and differentiation of the cell types. Methods: In this study, we present scGEM, a nested tree-structured nonparametric Bayesian model, to reveal the gene co-expression modules (GEMs) reflecting transcriptome processes in single cells. Results: We show that scGEM can discover shared and specialized transcriptome signals across different cell types using peripheral blood mononuclear single cells and early brain development single cells. scGEM outperformed other methods in perplexity and topic coherence (p < 0.001) on our simulation data. Larger datasets, deeper trees and pre-trained models are shown to be positively associated with better scGEM performance. The GEMs obtained from triple-negative breast cancer single cells exhibited better correlations with lymphocyte infiltration (p = 0.009) and the cell cycle (p < 0.001) than other methods in additional validation on the bulk RNAseq dataset. Conclusions: Altogether, we demonstrate that scGEM can be used to model the hidden cellular functions of single cells, thereby unveiling the specialization and generalization of transcriptomic programs across different types of cells.

APA, Harvard, Vancouver, ISO, and other styles

5

Algabri, Yousif A., Lingyu Li, and Zhi-Ping Liu. "scGENA: A Single-Cell Gene Coexpression Network Analysis Framework for Clustering Cell Types and Revealing Biological Mechanisms." Bioengineering 9, no. 8 (July 30, 2022): 353. http://dx.doi.org/10.3390/bioengineering9080353.

Full text

Abstract:

Single-cell RNA-sequencing (scRNA-seq) is a recent high-throughput technique that can measure gene expression, reveal cell heterogeneity, rare and complex cell populations, and discover cell types and their relationships. The analysis of scRNA-seq data is challenging because of transcripts sparsity, replication noise, and outlier cell populations. A gene coexpression network (GCN) analysis effectively deciphers phenotypic differences in specific states by describing gene–gene pairwise relationships. The underlying gene modules with different coexpression patterns partially bridge the gap between genotype and phenotype. This study presents a new framework called scGENA (single-cell gene coexpression network analysis) for GCN analysis based on scRNA-seq data. Although there are several methods for scRNA-seq data analysis, we aim to build an integrative pipeline for several purposes that cover primary data preprocessing, including data exploration, quality control, normalization, imputation, and dimensionality reduction of clustering as downstream of GCN analysis. To demonstrate this integrated workflow, an scRNA-seq dataset of the human diabetic pancreas with 1600 cells and 39,851 genes was implemented to perform all these processes in practice. As a result, scGENA is demonstrated to uncover interesting gene modules behind complex diseases, which reveal biological mechanisms. scGENA provides a state-of-the-art method for gene coexpression analysis for scRNA-seq data.

APA, Harvard, Vancouver, ISO, and other styles

6

Morii, Hiroshi, and Nozomu Mori. "Distribution of mRNA encoding SCG10 family (SCG10, RB3, and SCLIP) in rat brain." Neuroscience Research 31 (January 1998): S129. http://dx.doi.org/10.1016/s0168-0102(98)82014-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Youssef, Julie R., Nabila A. Boraie, Heba F. Ibrahim, Fatma A. Ismail, and Riham M. El-Moslemany. "Glibenclamide Nanocrystal-Loaded Bioactive Polymeric Scaffolds for Skin Regeneration: In Vitro Characterization and Preclinical Evaluation." Pharmaceutics 13, no. 9 (September 14, 2021): 1469. http://dx.doi.org/10.3390/pharmaceutics13091469.

Full text

Abstract:

Skin restoration following full-thickness injury poses significant clinical challenges including inflammation and scarring. Medicated scaffolds formulated from natural bioactive polymers present an attractive platform for promoting wound healing. Glibenclamide was formulated in collagen/chitosan composite scaffolds to fulfill this aim. Glibenclamide was forged into nanocrystals with optimized colloidal properties (particle size of 352.2 nm, and polydispersity index of 0.29) using Kolliphor as a stabilizer to allow loading into the hydrophilic polymeric matrix. Scaffolds were prepared by the freeze drying method using different total polymer contents (3–6%) and collagen/chitosan ratios (0.25–2). A total polymer content of 3% at a collagen/chitosan ratio of 2:1 (SCGL3-2) was selected based on the results of in vitro characterization including the swelling index (1095.21), porosity (94.08%), mechanical strength, rate of degradation and in vitro drug release. SCGL3-2 was shown to be hemocompatible based on the results of protein binding, blood clotting and percentage hemolysis assays. In vitro cell culture studies on HSF cells demonstrated the biocompatibility of nanocrystals and SCGL3-2. In vivo studies on a rat model of a full-thickness wound presented rapid closure with enhanced histological and immunohistochemical parameters, revealing the success of the scaffold in reducing inflammation and promoting wound healing without scar formation. Hence, SCGL3-2 could be considered a potential dermal substitute for skin regeneration.

APA, Harvard, Vancouver, ISO, and other styles

8

Lin, Chun-Chung, Kai-Pi Cheng, Hao-Chang Hung, Chung-Hao Li, Ching-Han Lin, Chih-Jen Chang, Che-Yuan Hu, Hung-Tsung Wu, and Horng-Yih Ou. "Serum Secretogranin III Concentrations Were Increased in Subjects with Metabolic Syndrome and Independently Associated with Fasting Plasma Glucose Levels." Journal of Clinical Medicine 8, no. 9 (September 11, 2019): 1436. http://dx.doi.org/10.3390/jcm8091436.

Full text

Abstract:

Secretogranin III (SCG3) plays a crucial role in the biogenesis of secretory granules in endocrine cells, and thus affects glucose homeostasis by regulating insulin secretion by pancreatic beta cells. Insulin resistance and compensatory hyperinsulinemia are hallmarks of metabolic syndrome (MetS). However, the role of SCG3 in MetS remains unclear. Therefore, we investigated the relationship between serum SCG3 levels and metabolic parameters in subjects with and without MetS. This was a case control study, and 295 subjects were recruited. Serum SCG3 concentrations were compared between groups. Associations between SCG3 levels and clinico-metabolic parameters were also examined. We found serum SCG3 levels were higher in the MetS group than non-MetS group (122.6 ± 79.2 vs. 90.6 ± 58.5 nmol/L, p = 0.009). Specifically, elevated SCG3 levels were found in subjects with high fasting plasma glucose (FPG) levels, central obesity, or hypertriglyceridemia. Additionally, MetS was an independent factor of serum SCG3 levels in multivariate linear regression analyses. Moreover, FPG, free fatty acids, and waist circumference were positively associated with serum SCG3 concentrations after adjusting for insulin levels, high-sensitivity C-reactive protein, and cardiovascular risk factors. In conclusion, serum SCG3 concentrations were higher in subjects with MetS and were independently associated with FPG levels.

APA, Harvard, Vancouver, ISO, and other styles

9

Hotta, Kikuko, Masahiro Hosaka, Atsushi Tanabe, and Toshiyuki Takeuchi. "Secretogranin II binds to secretogranin III and forms secretory granules with orexin, neuropeptide Y, and POMC." Journal of Endocrinology 202, no. 1 (April 8, 2009): 111–21. http://dx.doi.org/10.1677/joe-08-0531.

Full text

Abstract:

Functional variations in the secretogranin III (SCG3) gene are associated with susceptibility to obesity. SCG3 forms secretory granules with orexin, melanin-concentrating hormone (MCH), neuropeptide Y (NPY), and POMC in the hypothalamus. In this study, we screened proteins for SCG3-binding activity and identified secretogranin II (SCG2) using a yeast two-hybrid system. Immunoprecipitation revealed that SCG2 interacts with SCG3. In situ hybridization and immunohistochemistry indicated that SCG2 was highly expressed in the lateral hypothalamic area, paraventricular nucleus, and arcuate nucleus of the hypothalamus. Double-labeling immunohistochemical analysis demonstrated that SCG2 was expressed in orexin-, MCH-, NPY-, and POMC-expressing neurons. SCG2 was also coexpressed with SCG3. Upon introduction into neuroblastoma cells, SCG2 was expressed in the cytosol and formed granule-like structures with SCG3, orexin, NPY, or POMC. SCG3 bound to POMC; however, it did not bind to orexin, MCH, or NPY. By contrast, SCG2 formed aggregates with orexin, MCH, NPY, and POMC. SCG2 may act as a hormone carrier for orexin, MCH, NPY, and POMC by binding with SCG3, which targets proteins to the secretory granules. SCG2 mRNA levels increased along with those of SCG3, orexin, MCH, and NPY after a 24-h fast, suggesting that the SCG2/SCG3 system may respond in an adaptive manner to acute body weight changes. However, this SCG2/SCG3 system appears to be unresponsive to chronic body weight changes, such as diet-induced obesity or obesity in ob/ob mice. We suggest that SCG2, as well as SCG3, may be a potential regulator of food intake based on its capacity to accumulate appetite-related hormones into secretory granules.

APA, Harvard, Vancouver, ISO, and other styles

10

Nixon, Andrew B., Gabriele Grenningloh, and Patrick J. Casey. "The Interaction of RGSZ1 with SCG10 Attenuates the Ability of SCG10 to Promote Microtubule Disassembly." Journal of Biological Chemistry 277, no. 20 (March 6, 2002): 18127–33. http://dx.doi.org/10.1074/jbc.m201065200.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Lotfollahi, Mohammad, F. Alexander Wolf, and Fabian J. Theis. "scGen predicts single-cell perturbation responses." Nature Methods 16, no. 8 (July 29, 2019): 715–21. http://dx.doi.org/10.1038/s41592-019-0494-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Morii, H. "Activity-dependent protein phosphorylation of SCG10." Neuroscience Research 38 (2000): S104. http://dx.doi.org/10.1016/s0168-0102(00)81470-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Alves, Maria M., Grzegorz Burzynski, Jean-Marie Delalande, Jan Osinga, Annemieke van der Goot, Amalia M. Dolga, Esther de Graaff, et al. "KBP interacts with SCG10, linking Goldberg–Shprintzen syndrome to microtubule dynamics and neuronal differentiation." Human Molecular Genetics 19, no. 18 (July 9, 2010): 3642–51. http://dx.doi.org/10.1093/hmg/ddq280.

Full text

Abstract:

Abstract Goldberg–Shprintzen syndrome (GOSHS) is a rare clinical disorder characterized by central and enteric nervous system defects. This syndrome is caused by inactivating mutations in the Kinesin Binding Protein (KBP) gene, which encodes a protein of which the precise function is largely unclear. We show that KBP expression is up-regulated during neuronal development in mouse cortical neurons. Moreover, KBP-depleted PC12 cells were defective in nerve growth factor-induced differentiation and neurite outgrowth, suggesting that KBP is required for cell differentiation and neurite development. To identify KBP interacting proteins, we performed a yeast two-hybrid screen and found that KBP binds almost exclusively to microtubule associated or related proteins, specifically SCG10 and several kinesins. We confirmed these results by validating KBP interaction with one of these proteins: SCG10, a microtubule destabilizing protein. Zebrafish studies further demonstrated an epistatic interaction between KBP and SCG10 in vivo . To investigate the possibility of direct interaction between KBP and microtubules, we undertook co-localization and in vitro binding assays, but found no evidence of direct binding. Thus, our data indicate that KBP is involved in neuronal differentiation and that the central and enteric nervous system defects seen in GOSHS are likely caused by microtubule-related defects.

APA, Harvard, Vancouver, ISO, and other styles

14

Poulain, Fabienne E., and André Sobel. "The “SCG10-LIke Protein” SCLIP is a novel regulator of axonal branching in hippocampal neurons, unlike SCG10." Molecular and Cellular Neuroscience 34, no. 2 (February 2007): 137–46. http://dx.doi.org/10.1016/j.mcn.2006.10.012.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Tanabe, Atsushi, Takahiro Yanagiya, Aritoshi Iida, Susumu Saito, Akihiro Sekine, Atsushi Takahashi, Takahiro Nakamura, et al. "Functional Single-Nucleotide Polymorphisms in the Secretogranin III (SCG3) Gene that Form Secretory Granules with Appetite-Related Neuropeptides Are Associated with Obesity." Journal of Clinical Endocrinology & Metabolism 92, no. 3 (March 1, 2007): 1145–54. http://dx.doi.org/10.1210/jc.2006-1808.

Full text

Abstract:

Abstract Context: Genetic factors are important for the development of obesity. However, the genetic background of obesity still remains unclear. Objective: Our objective was to search for obesity-related genes using a large number of gene-based single-nucleotide polymorphisms (SNPs). Design and Setting: We conducted case-control association analyses using 94 obese patients and 658 controls with 62,663 SNPs selected from the SNP database. SNPs that possessed P ≤ 0.02 were further analyzed using 796 obese and 711 control subjects. One SNP (rs3764220) in the secretogranin III (SCG3) gene showed the lowest P value (P = 0.0000019). We sequenced an approximately 300-kb genomic region around rs3764220 and discovered SNPs for haplotype analyses. SCG3 was the only gene within a haplotype block that contained rs3764220. The functions of SCG3 were studied. Patients: Obese subjects (body mass index ≥ 30 kg/m2, n = 890) and control subjects (general population; n = 658, body mass index ≤ 25kg/m2; n = 711) were recruited for this study. Results: Twelve SNPs in the SCG3 gene including rs3764220 were in almost complete linkage disequilibrium and significantly associated with an obesity phenotype. Two SNPs (rs16964465, rs16964476) affected the transcriptional activity of SCG3, and subjects with the minor allele seemed to be resistant to obesity (odds ratio, 9.23; 95% confidence interval, 2.77–30.80; χ2 = 19.2; P = 0.0000067). SCG3 mRNA and immunoreactivity were detected in the paraventricular nucleus, lateral hypothalamic area, and arcuate nucleus, and the protein coexisted with orexin, melanin-concentrating hormone, neuropeptide Y, and proopiomelanocortin. SCG3 formed a granule-like structure together with these neuropeptides. Conclusions: Genetic variations in the SCG3 gene may influence the risk of obesity through possible regulation of hypothalamic neuropeptide secretion.

APA, Harvard, Vancouver, ISO, and other styles

16

Ji, Liyang, Prabuddha Waduge, Yan Wu, Chengchi Huang, Avinash Kaur, Paola Oliveira, Hong Tian, et al. "Secretogranin III Selectively Promotes Vascular Leakage in the Deep Vascular Plexus of Diabetic Retinopathy." International Journal of Molecular Sciences 24, no. 13 (June 23, 2023): 10531. http://dx.doi.org/10.3390/ijms241310531.

Full text

Abstract:

Diabetic retinopathy (DR), a leading cause of vision loss in working-age adults, induces mosaic patterns of vasculopathy that may be associated with spatial heterogeneity of intraretinal endothelial cells. We recently reported that secretogranin III (Scg3), a neuron-derived angiogenic and vascular leakage factor, selectively binds retinal vessels of diabetic but not healthy mice. Here, we investigated endothelial heterogeneity of three retinal vascular plexuses in DR pathogenesis and the therapeutic implications. Our unique in vivo ligand binding assay detected a 22.7-fold increase in Scg3 binding to retinal vessels of diabetic mice relative to healthy mice. Functional immunohistochemistry revealed that Scg3 predominantly binds to the DR-stressed CD31− deep retinal vascular plexus but not to the relatively healthy CD31+ superficial and intermediate plexuses within the same diabetic retina. In contrast, VEGF bound to healthy and diabetic retinal vessels indiscriminately with low activity. FITC-dextran assays indicated that selectively increased retinal vascular leakage coincides with Scg3 binding in diabetic mice that was independent of VEGF, whereas VEGF-induced leakage did not distinguish between diabetic and healthy mice. Dose–response curves showed that the anti-Scg3 humanized antibody (hAb) and anti-VEGF aflibercept alleviated DR leakage with equivalent efficacies, and that the combination acted synergistically. These findings suggest: (i) the deep plexus is highly sensitive to DR; (ii) Scg3 binding to the DR deep plexus coincides with the loss of CD31 and compromised endothelial junctions; (iii) anti-Scg3 hAb alleviates vascular leakage by selectively targeting the DR-stressed deep plexus within the same diabetic retina; (iv) combined anti-Scg3 and anti-VEGF treatments synergistically ameliorate DR through distinct mechanisms.

APA, Harvard, Vancouver, ISO, and other styles

17

He, Ye, Hong Tian, Chang Dai, Rong Wen, Xiaorong Li, Keith A. Webster, and Wei Li. "Optimal Efficacy and Safety of Humanized Anti-Scg3 Antibody to Alleviate Oxygen-Induced Retinopathy." International Journal of Molecular Sciences 23, no. 1 (December 29, 2021): 350. http://dx.doi.org/10.3390/ijms23010350.

Full text

Abstract:

The retinopathy of prematurity (ROP), a neovascular retinal disorder presenting in premature infants, is the leading causes of blindness in children. Currently, there is no approved drug therapy for ROP in the U.S., highlighting the urgent unmet clinical need for a novel therapeutic to treat the disease. Secretogranin III (Scg3) was recently identified as a disease-selective angiogenic factor, and Scg3-neutralizing monoclonal antibodies were reported to alleviate pathological retinal neovascularization in mouse models. In this study, we characterized the efficacy and safety of a full-length humanized anti-Scg3 antibody (hAb) to ameliorate retinal pathology in oxygen-induced retinopathy (OIR) mice, a surrogate model of ROP, by implementing histological and functional analyses. Our results demonstrate that the anti-Scg3 hAb outperforms the vascular endothelial growth factor inhibitor aflibercept in terms of efficacy and safety to treat OIR mice. Our findings support the development of anti-Scg3 hAb for clinical application.

APA, Harvard, Vancouver, ISO, and other styles

18

LeBlanc, Michelle E., Weiwen Wang, Xiuping Chen, Nora B. Caberoy, Feiye Guo, Chen Shen, Yanli Ji, et al. "Secretogranin III as a disease-associated ligand for antiangiogenic therapy of diabetic retinopathy." Journal of Experimental Medicine 214, no. 4 (March 22, 2017): 1029–47. http://dx.doi.org/10.1084/jem.20161802.

Full text

Abstract:

Diabetic retinopathy (DR) is a leading cause of vision loss with retinal vascular leakage and/or neovascularization. Current antiangiogenic therapy against vascular endothelial growth factor (VEGF) has limited efficacy. In this study, we applied a new technology of comparative ligandomics to diabetic and control mice for the differential mapping of disease-related endothelial ligands. Secretogranin III (Scg3) was discovered as a novel disease-associated ligand with selective binding and angiogenic activity in diabetic but not healthy vessels. In contrast, VEGF bound to and induced angiogenesis in both diabetic and normal vasculature. Scg3 and VEGF signal through distinct receptor pathways. Importantly, Scg3-neutralizing antibodies alleviated retinal vascular leakage in diabetic mice with high efficacy. Furthermore, anti-Scg3 prevented retinal neovascularization in oxygen-induced retinopathy mice, a surrogate model for retinopathy of prematurity (ROP). ROP is the most common cause of vision impairment in children, with no approved drug therapy. These results suggest that Scg3 is a promising target for novel antiangiogenic therapy of DR and ROP.

APA, Harvard, Vancouver, ISO, and other styles

19

Shalom, Hadas Sar, and Avraham Yaron. "Marking axonal growth in sensory neurons: SCG10." Experimental Neurology 254 (April 2014): 68–69. http://dx.doi.org/10.1016/j.expneurol.2014.01.014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Zou, Wenhui, Peixia Lin, Zhennan Zhao, Dongjiao Wang, Liqian Qin, Fu Xu, Yachun Su, Qibin Wu, and Youxiong Que. "Genome-Wide Identification of Auxin-Responsive GH3 Gene Family in Saccharum and the Expression of ScGH3-1 in Stress Response." International Journal of Molecular Sciences 23, no. 21 (October 22, 2022): 12750. http://dx.doi.org/10.3390/ijms232112750.

Full text

Abstract:

Gretchen Hagen3 (GH3), one of the three major auxin-responsive gene families, is involved in hormone homeostasis in vivo by amino acid splicing with the free forms of salicylic acid (SA), jasmonic acid (JA) or indole-3-acetic acid (IAA). Until now, the functions of sugarcane GH3 (SsGH3) family genes in response to biotic stresses have been largely unknown. In this study, we performed a systematic identification of the SsGH3 gene family at the genome level and identified 41 members on 19 chromosomes in the wild sugarcane species, Saccharum spontaneum. Many of these genes were segmentally duplicated and polyploidization was the main contributor to the increased number of SsGH3 members. SsGH3 proteins can be divided into three major categories (SsGH3-I, SsGH3-II, and SsGH3-III) and most SsGH3 genes have relatively conserved exon-intron arrangements and motif compositions. Diverse cis-elements in the promoters of SsGH3 genes were predicted to be essential players in regulating SsGH3 expression patterns. Multiple transcriptome datasets demonstrated that many SsGH3 genes were responsive to biotic and abiotic stresses and possibly had important functions in the stress response. RNA sequencing and RT-qPCR analysis revealed that SsGH3 genes were differentially expressed in sugarcane tissues and under Sporisorium scitamineum stress. In addition, the SsGH3 homolog ScGH3-1 gene (GenBank accession number: OP429459) was cloned from the sugarcane cultivar (Saccharum hybrid) ROC22 and verified to encode a nuclear- and membrane-localization protein. ScGH3-1 was constitutively expressed in all tissues of sugarcane and the highest amount was observed in the stem pith. Interestingly, it was down-regulated after smut pathogen infection but up-regulated after MeJA and SA treatments. Furthermore, transiently overexpressed Nicotiana benthamiana, transduced with the ScGH3-1 gene, showed negative regulation in response to the infection of Ralstonia solanacearum and Fusarium solani var. coeruleum. Finally, a potential model for ScGH3-1-mediated regulation of resistance to pathogen infection in transgenic N. benthamiana plants was proposed. This study lays the foundation for a comprehensive understanding of the sequence characteristics, structural properties, evolutionary relationships, and expression of the GH3 gene family and thus provides a potential genetic resource for sugarcane disease-resistance breeding.

APA, Harvard, Vancouver, ISO, and other styles

21

Huang, Chengchi, Liyang Ji, Avinash Kaur, Hong Tian, Prabuddha Waduge, Keith A. Webster, and Wei Li. "Anti-Scg3 Gene Therapy to Treat Choroidal Neovascularization in Mice." Biomedicines 11, no. 7 (July 6, 2023): 1910. http://dx.doi.org/10.3390/biomedicines11071910.

Full text

Abstract:

Neovascular age-related macular degeneration (nAMD) with choroidal neovascularization (CNV) is a leading cause of blindness in the elderly in developed countries. The disease is currently treated with anti-angiogenic biologics, including aflibercept, against vascular endothelial growth factor (VEGF) but with limited efficacy, treatment resistance and requirement for frequent intravitreal injections. Although anti-VEGF gene therapy may provide sustained therapy that obviates multiple injections, the efficacy and side effects related to VEGF pathway targeting remain, and alternative strategies to block angiogenesis independently of VEGF are needed. We recently reported that secretogranin III (Scg3) induces only pathological angiogenesis through VEGF-independent pathways, and Scg3-neutralizing antibodies selectively inhibit pathological but not physiological angiogenesis in mouse proliferative retinopathy models. Anti-Scg3 antibodies synergize dose-dependently with VEGF inhibitors in a CNV model. Here, we report that an adeno-associated virus-8 (AAV8) vector expressing anti-Scg3 Fab ameliorated CNV with an efficacy similar to that of AAV-aflibercept in a mouse model. This study is the first to test an anti-angiogenic gene therapy protocol that selectively targets pathological angiogenesis via a VEGF-independent mechanism. The findings support further safety/efficacy studies of anti-Scg3 gene therapy as monotherapy or combined with anti-VEGF to treat nAMD.

APA, Harvard, Vancouver, ISO, and other styles

22

Liu, Zhengyu, Tapan K. Chatterjee, and Rory A. Fisher. "RGS6 Interacts with SCG10 and Promotes Neuronal Differentiation." Journal of Biological Chemistry 277, no. 40 (July 24, 2002): 37832–39. http://dx.doi.org/10.1074/jbc.m205908200.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Ivanushko, A., Z. Shpyrka, N. German, and P. Demchenko. "ScGe2–RGe2 sections (R – La, Sm, Gd, Tb)." Visnyk of the Lviv University. Series Chemistry 64, no. 1 (2023): 26. http://dx.doi.org/10.30970/vch.6401.026.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Gavet, O., S. Ozon, V. Manceau, S. Lawler, P. Curmi, and A. Sobel. "The stathmin phosphoprotein family: intracellular localization and effects on the microtubule network." Journal of Cell Science 111, no. 22 (November 15, 1998): 3333–46. http://dx.doi.org/10.1242/jcs.111.22.3333.

Full text

Abstract:

Stathmin is a small regulatory phosphoprotein integrating diverse intracellular signaling pathways. It is also the generic element of a protein family including the neural proteins SCG10, SCLIP, RB3 and its two splice variants RB3′ and RB3″. Stathmin itself was shown to interact in vitro with tubulin in a phosphorylation-dependent manner, sequestering free tubulin and hence promoting microtubule depolymerization. We investigated the intracellular distribution and tubulin depolymerizing activity in vivo of all known members of the stathmin family. Whereas stathmin is not associated with interphase microtubules in HeLa cells, a fraction of it is concentrated at the mitotic spindle. We generated antisera specific for stathmin phosphoforms, which allowed us to visualize the regulation of phosphorylation-dephosphorylation during the successive stages of mitosis, and the partial localization of stathmin phosphorylated on serine 16 at the mitotic spindle. Results from overexpression experiments of wild-type and novel phosphorylation site mutants of stathmin further suggest that it induces depolymerization of interphase and mitotic microtubules in its unphosphorylated state but is inactivated by phosphorylation in mitosis. Phosphorylation of mutants 16A25A and 38A63A on sites 38 and 63 or 16 and 25, respectively, was sufficient for the formation of a functional spindle, whereas mutant 16A25A38A63E retained a microtubule depolymerizing activity. Transient expression of each of the neural phosphoproteins of the stathmin family showed that they are at least partially associated to the Golgi apparatus and not to other major membrane compartments, probably through their different NH2-terminal domains, as described for SCG10. Most importantly, like stathmin and SCG10, overexpressed SCLIP, RB3 and RB3″ were able to depolymerize interphase microtubules. Altogether, our results demonstrate in vivo the functional conservation of the stathmin domain within each protein of the stathmin family, with a microtubule destabilizing activity most likely essential for their specific biological function(s).

APA, Harvard, Vancouver, ISO, and other styles

25

Iwamaru, Yoshifumi, Hiroshi Kitani, Hiroyuki Okada, Takato Takenouchi, Yoshihisa Shimizu, Morikazu Imamura, Kohtaro Miyazawa, Yuichi Murayama, Edward A. Hoover, and Takashi Yokoyama. "Proximity of SCG10 and prion protein in membrane rafts." Journal of Neurochemistry 136, no. 6 (December 27, 2015): 1204–18. http://dx.doi.org/10.1111/jnc.13488.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Alves, Maria M. M., Jan Osinga, Joke B. G. M. Verheij, Marco Metzger, Bart J. L. Eggen, and Robert M. W. Hofstra. "Mutations in SCG10 Are Not Involved in Hirschsprung Disease." PLoS ONE 5, no. 12 (December 20, 2010): e15144. http://dx.doi.org/10.1371/journal.pone.0015144.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Shin, Jung Eun, Stefanie Geisler, and Aaron DiAntonio. "Dynamic regulation of SCG10 in regenerating axons after injury." Experimental Neurology 252 (February 2014): 1–11. http://dx.doi.org/10.1016/j.expneurol.2013.11.007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Guo, Q., N. Su, J. Zhang, X. Li, Z. Miao, G. Wang, M. Cheng, H. Xu, L. Cao, and F. Li. "PAK4 kinase-mediated SCG10 phosphorylation involved in gastric cancer metastasis." Oncogene 33, no. 25 (July 29, 2013): 3277–87. http://dx.doi.org/10.1038/onc.2013.296.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Antonsson, Bruno, Daniel B. Kassel, Gilbert Di Paolo, Robert Lutjens, Beat M. Riederer, and Gabriele Grenningloh. "Identification ofin VitroPhosphorylation Sites in the Growth Cone Protein SCG10." Journal of Biological Chemistry 273, no. 14 (April 3, 1998): 8439–46. http://dx.doi.org/10.1074/jbc.273.14.8439.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Shin, J. E., B. R. Miller, E. Babetto, Y. Cho, Y. Sasaki, S. Qayum, E. V. Russler, V. Cavalli, J. Milbrandt, and A. DiAntonio. "SCG10 is a JNK target in the axonal degeneration pathway." Proceedings of the National Academy of Sciences 109, no. 52 (November 27, 2012): E3696—E3705. http://dx.doi.org/10.1073/pnas.1216204109.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Iwata, T. "Alteration of SCG10 family mRNA expression after peripheral motoneuron injury." Neuroscience Research 38 (2000): S141. http://dx.doi.org/10.1016/s0168-0102(00)81693-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Pluzhnikov, V. B., A. Czopnik, and I. V. Svechkarev. "de Haas-van Alphen effect in ScGa3, LuGa3 and YIn3." Physica B: Condensed Matter 212, no. 4 (September 1995): 375–78. http://dx.doi.org/10.1016/0921-4526(95)00382-j.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Sobczak, Adam, Katarzyna Debowska, Magdalena Blazejczyk, Michael R. Kreutz, Jacek Kuznicki, and Urszula Wojda. "Calmyrin1 binds to SCG10 protein (stathmin2) to modulate neurite outgrowth." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1813, no. 5 (May 2011): 1025–37. http://dx.doi.org/10.1016/j.bbamcr.2010.12.023.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Togano, Tetsuya, Masashi Kurachi, Michitoshi Watanabe, Gabriele Grenningloh, and Michihiro Igarashi. "Role of Ser50 phosphorylation in SCG10 regulation of microtubule depolymerization." Journal of Neuroscience Research 80, no. 4 (May 15, 2005): 475–80. http://dx.doi.org/10.1002/jnr.20462.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Han, Jun Song, Xin Lu Lv, Ya Li Gao, Xiang Gao, and De Qi Xiong. "Analysis of DNA Damages of Gonadal Cells of Hemicentrotus pulcherrimus in Petroleum Hydrocarbons." Applied Mechanics and Materials 522-524 (February 2014): 251–56. http://dx.doi.org/10.4028/www.scientific.net/amm.522-524.251.

Full text

Abstract:

The single cell gel electrophoresis (SCGE) is a rapid and sensitive procedure for measuring strand breaks in DNA. In the present study, sea urchin (Hemicentrotus pulcherrimus) was chosen as the test organism and SCGE was applied to assess DNA damage of its gonadal cells exposed to petroleum hydrocarbon. The gonadal cells of sea urchin had been seriously damaged above 50 mg/L of Water Accommodated Fractions (WAFs), whileas no damages occurred in the lower concentrations. There were good linear relationships between exposure days and DNA damage rate, percentage of DNA in the comet tail (%TDNA) as well as comet tail length (TL).

APA, Harvard, Vancouver, ISO, and other styles

36

Groves, A. K., K. M. George, J. P. Tissier-Seta, J. D. Engel, J. F. Brunet, and D. J. Anderson. "Differential regulation of transcription factor gene expression and phenotypic markers in developing sympathetic neurons." Development 121, no. 3 (March 1, 1995): 887–901. http://dx.doi.org/10.1242/dev.121.3.887.

Full text

Abstract:

We have examined the regulation of transcription factor gene expression and phenotypic markers in developing chick sympathetic neurons. Sympathetic progenitor cells first express the bHLH transcriptional regulator Cash-1 (a chicken achaete-scute homologue), followed by coordinate expression of Phox2, a paired homeodomain protein, and GATA-2, a zinc finger protein. SCG10, a pan-neuronal membrane protein, is first detected one stage later, followed by the catecholaminergic neurotransmitter enzyme tyrosine hydroxylase (TH). We have used these markers to ask two questions: (1) is their expression dependent upon inductive signals derived from the notochord or floor plate?; (2) does their sequential expression reflect a single linear pathway or multiple parallel pathways? Notochord ablation experiments indicate that the floor plate is essential for induction of GATA-2, Phox2 and TH, but not for that of Cash-1 and SCG10. Taken together these data suggest that the development of sympathetic neurons involves multiple transcriptional regulatory cascades: one, dependent upon notochord or floor plate-derived signals and involving Phox2 and GATA-2, is assigned to the expression of the neurotransmitter phenotype; the other, independent of such signals and involving Cash-1, is assigned to the expression of pan-neuronal properties. The parallel specification of different components of the terminal neuronal phenotype is likely to be a general feature of neuronal development.

APA, Harvard, Vancouver, ISO, and other styles

37

Holmfeldt, Per, Kristoffer Brännström, Sonja Stenmark, and Martin Gullberg. "Deciphering the Cellular Functions of the Op18/Stathmin Family of Microtubule-Regulators by Plasma Membrane-targeted Localization." Molecular Biology of the Cell 14, no. 9 (September 2003): 3716–29. http://dx.doi.org/10.1091/mbc.e03-03-0126.

Full text

Abstract:

The Op18/stathmin family of microtubule regulators includes the ubiquitous cytosolic Op18/stathmin (Op18) and the neuronal, primarily Golgi-associated proteins SCG10 and RB3, which all form ternary complexes with two head-to-tail–aligned tubulin heterodimers. To understand the physiological significance of previously observed differences in ternary complex stability, we have fused each of the heterodimer-binding regions of these three proteins with the CD2 cell surface protein to generate confined plasma membrane localization of the resulting CD2 chimeras. Herein, we show that, in contrast to constitutively active CD2-Op18-tetraA, both the CD2-SCG10 and CD2-RB3 chimeras sequestered tubulin at the plasma membrane, which results in >35% reduction of cytosolic tubulin heterodimer levels and consequent delayed formation of mitotic spindles. However, all three CD2 chimeras, including the tubulin sequestration-incompetent CD2-Op18-tetraA, destabilize interphase microtubules. Given that microtubules are in extensive contact with the plasma membrane during interphase, but not during mitosis, these findings indicate that Op18-like proteins have the potential to destabilize microtubules by both sequestration and direct interaction with microtubules. However, the differences in tubulin binding observed in cells also indicate conceptual differences between the functions of low-abundance neural family members, which will accumulate tubulin at specific cellular compartments, and the abundant cytosolic Op18 protein, which will not.

APA, Harvard, Vancouver, ISO, and other styles

38

Hashem, Mohamed I., Zeeshan H. Ahmad, Mohammed A. Binmgren, Sukumaran Anil, and Sahar Bin Huraib. "Assessment of DNA Damage in Leukoplakia Patients with Different Degrees of Dysplasia." Journal of Contemporary Dental Practice 16, no. 12 (2015): 971–76. http://dx.doi.org/10.5005/jp-journals-10024-1790.

Full text

Abstract:

ABSTRACT Background Single cell gel electrophoresis (SCGE) assay also known as comet assay is a rapid and highly sensitive fluorescent molecular technique for detecting various forms of deoxyribonucleic acid (DNA) damage at individual cellular level. Materials and methods The present study was done to detect the extent of DNA damage in oral leukoplakia (OL) and compare with normal individuals. The sample population was obtained from an outpatient clinic of a tertiary teaching dental institute. A total of 36 consecutive patients with leukoplakia and 10 healthy normal volunteers were recruited for the study and assessed for the extent of DNA damage using SCGE following clinical diagnosis and histological grading. Peripheral blood was obtained by venipuncture and SCGE assay was performed. Mean comet tail length was recorded and analyzed statistically to compare the extent of damage in each group. Results The mean comet tail length seen in leukoplakia patients with moderate to severe dysplasia was 1.25 ± 0.14 mm while for the control subjects, it was 0.31 ± 0.10 mm. The difference was statistically significant (p = 0.000). On comparing within the grades of leukoplakia, a progressive trend of increasing tail length was observed with increasing grades of dysplasia. Conclusion Deoxyribonucleic acid damage as measured by SCGE is seen in leukoplakia. A stepwise increase in DNA damage levels from healthy controls, through patients with non-dysplastic epithelium to varying grades of dysplasia has been observed indicating the extent of DNA damage in this high risk group. How to cite this article Vellappally S, Binmgren MA, Huraib SB, Hashem MI, Patil S, Anil S. Assessment of DNA Damage in Leukoplakia Patients with Different Degrees of Dysplasia. J Contemp Dent Pract 2015;16(12):971-976.

APA, Harvard, Vancouver, ISO, and other styles

39

KOIKE, Atsushi, Takayuki UEDA, and Mitsuhiro MIYASHIT. "SCGE model for passenger transport improvement." INFRASTRUCTURE PLANNING REVIEW 17 (2000): 237–45. http://dx.doi.org/10.2208/journalip.17.237.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Kliemann, Mariele, Daniel Prá, Luiza L. Müller, Liziane Hermes, Jorge A. Horta, Miriam B. Reckziegel, Miria S. Burgos, Sharbel W. Maluf, Silvia I. R. Franke, and Juliana da Silva. "DNA damage in children and adolescents with cardiovascular disease risk factors." Anais da Academia Brasileira de Ciências 84, no. 3 (June 28, 2012): 833–40. http://dx.doi.org/10.1590/s0001-37652012005000039.

Full text

Abstract:

The risk of developing cardiovascular disease (CVD) is related to lifestyle (e.g. diet, physical activity and smoking) as well as to genetic factors. This study aimed at evaluating the association between CVD risk factors and DNA damage levels in children and adolescents. Anthropometry, diet and serum CVD risk factors were evaluated by standard procedures. DNA damage levels were accessed by the comet assay (Single cell gel electrophoresis; SCGE) and cytokinesis-blocked micronucleus (CBMN) assays in leukocytes. A total of 34 children and adolescents selected from a population sample were divided into three groups according to their level of CVD risk. Moderate and high CVD risk subjects showed significantly higher body fat and serum CVD risk markers than low risk subjects (P<0.05). High risk subjects also showed a significant increase in DNA damage, which was higher than that provided by low and moderate risk subjects according to SCGE, but not according to the CBMN assay. Vitamin C intake was inversely correlated with DNA damage by SCGE, and micronucleus (MN) was inversely correlated with folate intake. The present results indicate an increase in DNA damage that may be a consequence of oxidative stress in young individuals with risk factors for CVD, indicating that the DNA damage level can aid in evaluating the risk of CVD.

APA, Harvard, Vancouver, ISO, and other styles

41

Riederer, B. M., V. Pellier, B. Antonsson, G. Di Paolo, S. A. Stimpson, R. Lutjens, S. Catsicas, and G. Grenningloh. "Regulation of microtubule dynamics by the neuronal growth-associated protein SCG10." Proceedings of the National Academy of Sciences 94, no. 2 (January 21, 1997): 741–45. http://dx.doi.org/10.1073/pnas.94.2.741.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Matsuo, Naoki, Shoko Kawamoto, Kenichi Matsubara, and Kousaku Okubo. "A novel SCG10-related gene uniquely expressed in the nervous system." Gene 215, no. 2 (July 1998): 477–81. http://dx.doi.org/10.1016/s0378-1119(98)00324-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Tararuk, Tatsiana, Nina Östman, Wenrui Li, Benny Björkblom, Artur Padzik, Justyna Zdrojewska, Vesa Hongisto, et al. "Correction: JNK1 phosphorylation of SCG10 determines microtubule dynamics and axodendritic length." Journal of Cell Biology 173, no. 5 (June 5, 2006): 821. http://dx.doi.org/10.1083/jcb.20051105520060522c.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Okazaki, Takashi, Benton N. Yoshida, Karen B. Avraham, Haimei Wang, Carol W. Wuenschell, Nancy A. Jenkins, Neal G. Copeland, David J. Anderson, and Nozomu Mori. "Molecular Diversity of the SCG10/Stathmin Gene Family in the Mouse." Genomics 18, no. 2 (November 1993): 360–73. http://dx.doi.org/10.1006/geno.1993.1477.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Di Paolo, Gilbert, Robert Lutjens, Astrid Osen-Sand, Andr� Sobel, Stefan Catsicas, and Gabriele Grenningloh. "Differential distribution of stathmin and SCG10 in developing neurons in culture." Journal of Neuroscience Research 50, no. 6 (December 15, 1997): 1000–1009. http://dx.doi.org/10.1002/(sici)1097-4547(19971215)50:6<1000::aid-jnr10>3.0.co;2-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Ali Berber, Ahmet, Nurcan Berber, Ibrahim Uysal, and Nihan Akinci Kenanoglu. "EVALUATION OF CYTOTOXIC AND GENOTOXIC EFFECTS OF SAXAGLIPTIN." International Journal of Advanced Research 10, no. 06 (June 30, 2022): 216–22. http://dx.doi.org/10.21474/ijar01/14878.

Full text

Abstract:

Saxagliptin (SAX) is an oral drug that is a hypoglycemic (between an anti-diabetic agent) dipeptidyl peptidase-4 inhibitor. In this study, cytotoxic, genotoxic effects and DNA damage of SAX on human lymphocytes were investigated. For this purpose, Single Cell Gel Electrophoresis (SCGE), Micronucleus (MN) and Mitotic Index (MI) tests were used. Based on the daily doses of SAX, 0.017, 0.035, 0.07, 0.14 Âµg/mL concentrations used for the study. SAX significantly reduced the MI only at the highest concentration (0.14 Âµg/mL) for 24 hours, and 0.07- and 0.14-Âµg/mL concentrations for 48 hours. SAX did not cause a statistically significant change in MN frequency (except for concentration 0.14 Âµg/mL). In the SCGE test, a statistically significant increase of comet tail length was observed at 0.07- and 0.14-Âµg/mL concentrations. SAX did not cause a statistically significant change in comet tail moment and tail intensity (except for concentration 0.14 Âµg/mL). As a result, SAX caused statistically differences in the SCGE, MI and MN tests only at the highest concentrations that are not recommended commercial use (except for tail length, 0.035 Âµg/mL). When the results of all these studies are evaluated together, it can be said that SAX has no aneugenic, mutagenic and clastogenic effects at daily doses in in vitro studies on human lymphocytes.

APA, Harvard, Vancouver, ISO, and other styles

47

Sukhareva, S. I., D. A. Aristov, V. D. Gankevich, A. G. Desnitskiy, S. K. Ozman-Sullivan, and P. E. Chetverikov. "Synhospitality of eriophyoid mites (Acariformes, Eriophyoidea): taxonomic analysis of gall-forming mite species complexes on boreal woody dicotyledons." Паразитология 58, no. 2 (June 4, 2024): 101–23. http://dx.doi.org/10.31857/s0031184724020029.

Full text

Abstract:

Microscopic mites of the Eriophyoidea superfamily are characterized by an ability to cause the growth of galls on plants. Synhospital complexes of gall-forming Eriophyoidea (SCGE) species are formed by several species of gall mites coexisting on the same host plant. To assess the phenomenon of synhospitality, we investigated the features of the taxonomic composition and diversity of galls formed by eriophyoid mites on boreal woody dicotyledons and carried out a statistical analysis of the host relationships of different gall mite genera from the Eriophyidae family. We found out that phylogenetically closely related hosts within biogeographically integral territories possess the similar SCGE. During colonization of plants, gall mites demonstrate a high ability to cryptic speciation, which leads to genesis of morphologically similar mite species that cause the formation of different types of galls. Host preferences of gall mites belonging to the different supergenera groups play an important role in the formation of the SCGE, which determines the differences in mite taxa spectra associated with hosts from different families. In general, the results of the work demonstrate that the synhospitality of Eriophyoidea is not a random process, but is the result of a long-term coadaptation in the “parasite–host” system. This is one of the phenomena reflecting the stages of the global historical process of the colonization of Embriophyta plants by mites of the Eriophyoidea superfamily.

APA, Harvard, Vancouver, ISO, and other styles

48

Liu, Yonghua, Youhua Wang, Ying Chen, Xiaohong Li, Jiao Yang, Yang Liu, and Aiguo Shen. "Spy1 Protein Mediates Phosphorylation and Degradation of SCG10 Protein in Axonal Degeneration." Journal of Biological Chemistry 290, no. 22 (April 13, 2015): 13888–94. http://dx.doi.org/10.1074/jbc.m114.611574.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Burzynski, Grzegorz M., Jean-Marie Delalande, and Iain Shepherd. "Characterization of spatial and temporal expression pattern of SCG10 during zebrafish development." Gene Expression Patterns 9, no. 4 (April 2009): 231–37. http://dx.doi.org/10.1016/j.gep.2008.12.010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Liu, Yonghua, Youhua Wang, Ying Chen, Xiaohong Li, Jiao Yang, Yang Liu, and Aiguo Shen. "Spy1 protein mediates phosphorylation and degradation of SCG10 protein in axonal degeneration." Journal of Biological Chemistry 291, no. 44 (October 28, 2016): 23365. http://dx.doi.org/10.1074/jbc.a114.611574.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!