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Academic literature on the topic 'RLF receptor'

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Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "RLF receptor"

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Minagawa, Itaru, Masafumi Fukuda, Hisako Ishige, Hiroshi Kohriki, Masatoshi Shibata, Enoch Y. Park, Tatsuo Kawarasaki, and Tetsuya Kohsaka. "Relaxin-like factor (RLF)/insulin-like peptide 3 (INSL3) is secreted from testicular Leydig cells as a monomeric protein comprising three domains B–C–A with full biological activity in boars." Biochemical Journal 441, no. 1 (December 14, 2011): 265–73. http://dx.doi.org/10.1042/bj20111107.

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RLF (relaxin-like factor), also known as INSL3 (insulin-like peptide 3), is a novel member of the relaxin/insulin gene family that is expressed in testicular Leydig cells. Despite the implicated role of RLF/INSL3 in testis development, its native conformation remains unknown. In the present paper we demonstrate for the first time that boar testicular RLF/INSL3 is isolated as a monomeric structure with full biological activity. Using a series of chromatography steps, the native RLF/INSL3 was highly purified as a single peak in reverse-phase HPLC. MS/MS (tandem MS) analysis of the trypsinized sample provided 66% sequence coverage and revealed a distinct monomeric structure consisting of the B-, C- and A-domains deduced previously from the RLF/INSL3 cDNA. Moreover, the N-terminal peptide was four amino acid residues longer than predicted previously. MS analysis of the intact molecule and PMF (peptide mass fingerprinting) analysis at 100% sequence coverage confirmed this structure and indicated the existence of three site-specific disulfide bonds. RLF/INSL3 retained full bioactivity in HEK (human embryonic kidney)-293 cells expressing RXFP2 (relaxin/insulin-like family peptide receptor 2), the receptor for RLF/INSL3. Furthermore, RLF/INSL3 was found to be secreted from Leydig cells into testicular venous blood. Collectively, these results indicate that boar RLF/INSL3 is secreted from testicular Leydig cells as a B–C–A monomeric structure with full biological activity.
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Büllesbach, Erika E., and Christian Schwabe. "Tryptophan B27 in the Relaxin-like Factor (RLF) Is Crucial for RLF Receptor-Binding†." Biochemistry 38, no. 10 (March 1999): 3073–78. http://dx.doi.org/10.1021/bi982687u.

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Büllesbach, Erika E., Fredric R. Boockfor, George Fullbright, and Christian Schwabe. "Cryptorchidism induced in normal rats by the relaxin-like factor inhibitor." REPRODUCTION 135, no. 3 (March 2008): 351–55. http://dx.doi.org/10.1530/rep-07-0330.

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Cryptorchidism is a serious problem, which affects 2–5% of the male population. Failure of the testes to descend into the scrotal region impairs germ cell development and is associated with a greater incidence of testicular cancer. The relaxin-like factor (RLF or insulin-like-3) has been shown to be critically important for the timely descent of the testicles in mice. We have discovered that the signal initiation site of the RLF can be eliminated without measurable effects on hormone binding to its receptor and that the resulting RLF derivative is a competitive inhibitor of RLF called RLFi. RLFi administered to pregnant rats causes dose-dependent gonadal retention in the offspring. The ability to control the severity of the syndrome by altering the concentration of RLFi and the timing of administration enables us to study in detail the structural changes that are associated with the action of RLF during critical stages of development. Targeted inhibition of the physiological migration pattern of testicles by RLFi lets one dissect the physiological process such as to find a window for clinical application of RLF and to search for ancillary factors that might play a role during normal development.
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SIQIN, Mari NAKAI, Tomohiro HAGI, Shinichi KATO, Ali Mohammed PITIA, Mai KOTANI, Yuki ODANAKA, et al. "Partial cDNA sequence of a relaxin-like factor (RLF) receptor, LGR8 and possible existence of the RLF ligand-receptor system in goat testes." Animal Science Journal 81, no. 6 (October 29, 2010): 681–86. http://dx.doi.org/10.1111/j.1740-0929.2010.00801.x.

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Boockfor, F. "Relaxin-like factor (RLF) serum concentrations and gubernaculum RLF receptor display in relation to pre- and neonatal development of rats." Reproduction 122, no. 6 (December 1, 2001): 899–906. http://dx.doi.org/10.1530/reprod/122.6.899.

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Minagawa, Itaru, Dai Sagata, Ali Mohammed Pitia, Hiroshi Kohriki, Masatoshi Shibata, Hiroshi Sasada, Yoshihisa Hasegawa, and Tetsuya Kohsaka. "Dynamics of insulin-like factor 3 and its receptor expression in boar testes." Journal of Endocrinology 220, no. 3 (March 2014): 247–61. http://dx.doi.org/10.1530/joe-13-0430.

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Relaxin-like factor (RLF), now mainly known as insulin-like factor 3 (INSL3), is essential for testis descent during fetal development; however, its function in the adult testis is still being elucidated. As a major step toward understanding the as-yet-unknown function of INSL3 in boars, this study aimed to develop a time-resolved fluoroimmunoassay for boar INSL3, characterize the dynamics of INSL3 expression during development, and demonstrate the expression of the INSL3 hormone–receptor system in the testis. All samples were collected from Duroc boars. The sensitivity of the assay system established was 8.2 pg/well (164 pg/ml), and no cross-reactivity with other hormones, such as porcine relaxin, was observed. Circulating INSL3 was shown to increase progressively during development. INSL3 secreted from the Leydig cells was released not only into the blood circulation but also into the interstitial and seminiferous compartments in sufficient concentrations. A testicular fractionation study revealed that its receptor RXFP2 transcripts were expressed mainly in testicular germ cells. In addition, INSL3 bound to the germ cell membranes in a hormone-specific and saturable manner. These results reveal that INSL3 secreted into the interstitial compartment from the Leydig cells is transported into the seminiferous compartments, where its receptor RXFP2 is expressed mainly in the germ cells to which INSL3 binds, suggesting that INSL3 functions as a paracrine factor on seminiferous germ cells.
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Büllesbach, Erika E., and Christian Schwabe. "The Mode of Interaction of the Relaxin-like Factor (RLF) with the Leucine-rich Repeat G Protein-activated Receptor 8." Journal of Biological Chemistry 281, no. 36 (July 14, 2006): 26136–43. http://dx.doi.org/10.1074/jbc.m601414200.

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Post, Ginell R., Carol Swiderski, Bruce A. Waldrop, Lina Salty, Christopher C. Glembotski, Rob M. F. Wolthuis, and Naoki Mochizuki. "Guanine Nucleotide Exchange Factor-like Factor (Rlf) Induces Gene Expression and Potentiates α1-Adrenergic Receptor-induced Transcriptional Responses in Neonatal Rat Ventricular Myocytes." Journal of Biological Chemistry 277, no. 18 (February 14, 2002): 15286–92. http://dx.doi.org/10.1074/jbc.m111844200.

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Siqin, Itaru Minagawa, Mitsutoshi Okuno, Kimihiko Yamada, Yasushi Sugawara, Yoshio Nagura, Koh-Ichi Hamano, Enoch Y. Park, Hiroshi Sasada, and Tetsuya Kohsaka. "The active form of goat insulin-like peptide 3 (INSL3) is a single-chain structure comprising three domains B-C-A, constitutively expressed and secreted by testicular Leydig cells." Biological Chemistry 394, no. 9 (September 1, 2013): 1181–94. http://dx.doi.org/10.1515/hsz-2012-0357.

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Abstract Relaxin-like factor (RLF), also called insulin-like peptide 3 (INSL3), is a member of the insulin/relaxin gene family and is produced by testicular Leydig cells. While the understanding of its effects is growing, very little is known about the structural and functional properties of native INSL3. Here, we demonstrate that native INSL3 isolated from goat testes is a single-chain structure with full biological activity, and is constitutively expressed and secreted by Leydig cells. Using a series of chromatography steps, native INSL3 was highly purified as a single 12-kDa peak as revealed by SDS-PAGE. MS/MS analysis provided 81% sequence coverage and revealed a distinct single-chain structure consisting of the B-, C-, and A-domains deduced previously from the INSL3 cDNA sequence. Moreover, the N-terminal peptide was six amino acid residues longer than predicted. Native INSL3 exhibited full bioactivity in HEK-293 cells expressing the receptor for INSL3. Immunoelectron microscopy and Western blot analysis revealed that INSL3 was secreted by Leydig cells through the constitutive pathway into blood and body fluids. We conclude, therefore, that goat INSL3 is constitutively secreted from Leydig cells as a B-C-A single-chain structure with full biological activity.
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Antonelli, Valeria, Francesca Bernasconi, Yung H. Wong, and Lucia Vallar. "Activation of B-Raf and Regulation of the Mitogen-activated Protein Kinase Pathway by the Go α chain." Molecular Biology of the Cell 11, no. 4 (April 2000): 1129–42. http://dx.doi.org/10.1091/mbc.11.4.1129.

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Many receptors coupled to the pertussis toxin-sensitive Gi/o proteins stimulate the mitogen-activated protein kinase (MAPK) pathway. The role of the α chains of these G proteins in MAPK activation is poorly understood. We investigated the ability of Gαo to regulate MAPK activity by transient expression of the activated mutant Gαo-Q205L in Chinese hamster ovary cells. Gαo-Q205L was not sufficient to activate MAPK but greatly enhanced the response to the epidermal growth factor (EGF) receptor. This effect was not associated with changes in the state of tyrosine phosphorylation of the EGF receptor. Gαo-Q205L also potentiated MAPK stimulation by activated Ras. In Chinese hamster ovary cells, EGF receptors activate B-Raf but not Raf-1 or A-Raf. We found that expression of activated Gαo stimulated B-Raf activity independently of the activation of the EGF receptor or Ras. Inactivation of protein kinase C and inhibition of phosphatidylinositol-3 kinase abolished both B-Raf activation and EGF receptor-dependent MAPK stimulation by Gαo. Moreover, Gαo-Q205L failed to affect MAPK activation by fibroblast growth factor receptors, which stimulate Raf-1 and A-Raf but not B-Raf activity. These results suggest that Gαo can regulate the MAPK pathway by activating B-Raf through a mechanism that requires a concomitant signal from tyrosine kinase receptors or Ras to efficiently stimulate MAPK activity. Further experiments showed that receptor-mediated activation of Gαo caused a B-Raf response similar to that observed after expression of the mutant subunit. The finding that Gαo induces Ras-independent and protein kinase C- and phosphatidylinositol-3 kinase-dependent activation of B-Raf and conditionally stimulates MAPK activity provides direct evidence for intracellular signals connecting this G protein subunit to the MAPK pathway.
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Dissertations / Theses on the topic "RLF receptor"

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Nasa, Zeyad, and nasa zeyad@med monash edu au. "Characterization of the Rat Relaxin-like Factor Gene." RMIT University. Medical Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080514.100729.

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Relaxin-like factor (RLF), also known as Leydig insulin-like peptide (Ley-I-L) or Insulin 3 (INSL3), is a newly characterized member of the insulin peptide family. Amino acid sequence homology revealed that RLF is more closely related to relaxin than any other insulin-like hormones. The main aim of this thesis was to sequence the rat RLF (Relaxin-like factor) gene and determine the structure and organisation of the gene. Secondly to compare the structural organisation of the rat RLF/JAK3 genomic region with that of the mouse and human, using bioinformatic databases. Thirdly to further investigate the signalling pathways for the RLF receptor, in particular the NFƒÛB pathway. The homology between rat and mouse in the JAK3/RLF region revealed 84.4 % similarity over 1262 bp of DNA sequence, observing that unlike the mouse, the rat RLF promoter is separated from the JAK3 gene by around 700-1000 bp. Similarly in humans, the RLF gene is located around 4 kb downstre am from JAK3. Also Protein kinase A (PKA) was the only signalling pathway which dispalyed major induction and no inhibitory effects were observed through the NFƒÛB signalling pathway.
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Restrepo, Montoya Daniel. "Computational Identification, Phylogenetic and Synteny Analysis of Receptor-Like Kinases “RLK” and Receptor-Like Proteins “RLP” in Legumes." Diss., North Dakota State University, 2018. https://hdl.handle.net/10365/29870.

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Legumes are considered the second most important family of crop plants after the grass family based on economic relevance. In recent years, the field of legume genomics has expanded due to advancements in high-throughput sequencing and genotyping technologies. To date, no published comparative genomic analysis explores receptor-like kinases “RLK” and receptor-like proteins “RLP” among legume genomes. Evaluating these RLK and RLP should provide a source of new information because extensive genetic and phenotypic studies have already discovered the diverse roles of RLK and RLP in cell development, disease resistance, and stress responses among other functions. This study demonstrates that a computational logical approach for classifying the RLK/RLP in legumes/non-legumes is statistically well supported and can be used in other plant species. The analysis of RLK/RLP of 7 legumes and 3 non-legume species evaluated suggests that about 2% are RLK and less than 1% of the proteins are RLP. The results suggest a dynamic evolution of RLK and RLP in the legume family. In fact, between 66% to 85% of RLK and 83% to 88% of RLP belong to orthologous clusters among the species evaluated. The remaining RLK and RLP proteins are classified as singletons. The ratio of the pairwise synteny blocks of RLK/RLP among legumes shows a 1:1 relationship. The exception is G. max, which shows an approximately 2:1 ratio due to its recent whole genome duplication (G. max vs. the other six legumes). The other legumes show evidence of a similar proportion of plasma membrane proteins among the legume pairwise synteny blocks.
Fulbright Scholarship
Francisco Jose de Caldas (Colciencias, Colombia) Scholarship
North Dakota State University. Dry Breeding Program
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Marcu, Jahan Phillip. "Novel Insights into CB1 Receptor Signaling and the Anabolic Role of Cannabinoid Receptors in Bone." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/233543.

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Cell Biology
Ph.D.
Activation of the CB1 receptor is modulated by aspartate residue D2.63176 in transmembrane helix (TMH) II. Interestingly, D2.63 does not affect the affinity for ligand binding at the CB1 receptor. Studies in class A GPCRs have suggested an ionic interaction between residues of TMHII and VII. In this report, modeling studies identified residue K373, in the extracellular (EC)-3 loop, in charged interactions with D2.63. We investigated this possibility by performing reciprocal mutations and biochemical studies. D2.63176A, K373A, D2.63176A-K373A, and the reciprocal mutant with the interacting residues juxtaposed, D2.63176K-K373D were characterized using radioligand binding and guanosine 5'-3-O-(thio)triphosphate functional assays. None of the mutations resulted in a significant change in the binding affinity of CP55,940 or SR141716A. Computational results indicate that the D2.63176-K373 ionic interaction strongly influences the conformation(s) of the EC-3 loop, providing a structure-based rationale for the importance of the EC-3 loop to signal transduction in CB1. Specifically, the putative ionic interaction results in the EC-3 loop pulling over the top (extracellular side) of the receptor; this EC-3 loop conformation may serve protective and mechanistic roles. These results suggest that the ionic interaction between D2.63176 and K373 is crucial for CB1 signal transduction. This work may help to aide drug design efforts for the effective treatment of different diseases. The cannabinoid receptors of osteoblasts may represent a target for the treatment of bone disorders such as osteoporosis. Our research demonstrates that cannabinoids can affect important signaling molecules in osteoblasts. In MC3T3-E1 osteoblastic cells, the CB1 antagonist, AM251, has been reported to induce increases in Runx2 mRNA, mineralized bone nodule formation, and activation of signaling molecules such as ERK and AKT (Wu et al., 2011). Studies from our lab characterizing mice in which both CB1 and CB2 receptors were inactivated by homologous recombination have demonstrated increased bone mass coupled with enhanced osteoblast differentiation of bone marrow stromal cells in culture (manuscript in preparation). We explored the effect of antagonizing CB1 and CB2 cannabinoid receptors in osteoblastic cells to gain insights into molecular pathways that may help to explain the effects of the endocannabinoid system (ECS) in bone development. Our data was generated by running time course experiments with MC3T3-E1 cells under the influence of SR141716A, SR144528 or both in combination. The cells were harvested with a lysis buffer at specific time points and analyzed by western blot analysis. Quantification of protein activation was calculated using LiCor imaging equipment and software. Within 15 minutes, treatment with the CB1 receptor antagonist SR141716A resulted in several fold increases in pERK, pSMAD158, and pAKT. SR144528, a CB2 receptor antagonist, caused increases in pERK and pSMAD158, but not pAKT. When both antagonists were applied together, pERK and pSMAD158 levels increased, while pAKT signaling was diminished compared to SR141716A alone. The finding that cannabinoid receptor antagonists alter the activity of the SMAD158 complex is a novel finding, which suggests that cannabinoids can influence bone morphogenic signaling pathways, and therefore play a significant role in osteoblast differentiation and function.
Temple University--Theses
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Tumati, Suneeta. "Functional regulation of opioid receptor signaling." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/194989.

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Studies have shown that long-term opioid agonist (such as morphine) treatment produces antinociceptive tolerance and increased pain sensitivity (hyperalgesia and/or allodynia), limiting the clinical efficacy of morphine. Prolonged opiate administration also upregulates spinal pain neurotransmitter (such as calcitonin gene-related peptide (CGRP)) levels and enhances evoked CGRP release in the dorsal horn of rats. It was suggested that augmented spinal pain neurotransmission may contribute to paradoxical pain sensitization and antinociceptive tolerance. The cellular signal transduction pathways involved in sustained opioid mediated augmentation of spinal pain neurotransmitter are not fully clarified.Sustained morphine treatment was shown to augment the concentrations of inflammatory mediators, such as PGE2 in the spinal cord. Studies have shown that PGE2 stimulates cAMP formation and CGRP release by activation of Gs protein-coupled prostaglandin receptor types in primary sensory neurons. Interestingly, it was found earlier that sustained opioid agonist treatment leads to a Raf-1-dependent sensitization of adenylyl cyclase(s) (AC superactivation), augmenting forskolin-stimulated cAMP formation upon opioid withdrawal (cAMP overshoot). It is well demonstrated that cAMP activates cAMP-dependent protein kinase (PKA), which plays an important role in the modulation of presynaptic neurotransmitter release. Therefore, in this study, we investigate the physiological role of Raf-1 mediated AC superactivation and subsequent PKA activation in A. sustained morphine-mediated augmentation of basal or evoked pain neurotransmitter release in vitro, in cultured primary sensory neurons, and B. in vivo, in sustained morphine mediated paradoxical pain sensitization and antinociceptive tolerance in rats.Our data demonstrates that A. sustained morphine treatment augments both basal and capsaicin-evoked CGRP release from isolated primary sensory neurons in a PKA- and Raf-1- dependent manner. B. sustained morphine treatment- augments of PGE2-evoked CGRP release from these cells. C. selective knockdown of spinal PKA or Raf-1 protein levels by intrathecal PKA- or Raf-1-specific siRNA pretreatment completely attenuates sustained morphine-mediated thermal hyperalgesia, tactile allodynia and greatly reduces antinociceptive tolerance in rats.In conclusion, we suggest that Raf-1-mediated AC superactivation may have a crucial trigger role in sustained morphine-mediated compensatory adaptations in the nervous system. Thus, we expect that pharmacological attenuation of Raf-1-mediated AC superactivation may improve the clinical treatment of chronic and neuropathic pain.
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Chiu, Yi-Ting. "STUDIES ON NEURITE OUTGROWTH AND RECEPTOR PHOSPHORYLATION FOLLOWING KAPPA OPIOID RECEPTOR ACTIVATION." Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/384383.

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Pharmacology
Ph.D.
Kappa opioid receptor (KOPR) is involved in many physiological functions and pharmacological responses such as analgesia, anti-pruritic effect, sedation, motor incoordination and aversion (Simonin et al., 1998; Liu-Chen, 2004). The cellular mechanisms following activation of KOPR involve in part Gi/o protein-dependent pathways (Law et al., 2000). Following KOPR activation, the receptor is phosphorylated and arrestins are recruited. Arrestins mediate agonist-dependent KOPR desensitization, internalization and down-regulation (Liu-Chen, 2004). In recent years, arrestins were found to initiate arrestin-dependent downstream signaling. Thus, agonist-promoted KOPR phosphorylation plays a pivotal role in KOPR regulation and signaling. Previous studies from our lab showed that in Chinese hamster ovary (CHO) cells stably transfected with the human KOPR (hKOPR), U50,488H induced phosphorylation (Li et al., 2002a); however, sites of phosphorylation were not determined. Using LC-MS/MS, our lab recently identified four residues (S356, T357, T363 and S369) to be the sites of U50,488H-promoted phosphorylation in the mouse KOPR (mKOPR) stably expressed in N2A cells (Chen et al., 2016). Antibodies were generated against phosphopeptides and purified and three antibodies were found to have high specificity for the mKOPR phosphorylated at S356/T357, T363 and S369, respectively (Chen et al., 2016). Our lab previously showed that while U50,488H promoted robust hKOPR phosphorylation and internalization, etorphine induced little phosphorylation and internalization, although both were potent full agonists in enhancing [35S]GTPγS (Li et al., 2002a; Zhang et al., 2002; Li et al., 2003). Etorphine caused lower levels of KOPR phosphorylation at all the four residues than U50,488H by immunoblotting with the phospho-specific antibodies (Chen et al., 2016). Using the SILAC (stable isotope labeling by amino acids in cell culture) approach, we have found that compared to etorphine, U50,488H promoted higher levels of single phosphorylation at T363 and S369 and double phosphorylation at T363+S369 and T357+S369 as well as triple phosphorylation at S356+T357+S369 (Chen et al., 2016). These results indicate that an above-threshold phosphorylation is required for KOPR internalization. It has been reported that KOPR is involved in neuronal differentiation and neurogenesis. In the first chapter, I focused on whether there are differences in the mechanisms underlying neurite outgrowth induced by U50,488H and etorphine. In the chapter 2, mechanisms of KOPR phosphorylation were characterized in detail using phospho-specific KOPR antibodies. Protein kinase C was found, for the first time, to be involved in agonist-promoted KOPR phosphorylation. The roles of PKC in behavioral effects induced by KOPR agonists in mice were examined. For the chapter 1, in Neuro2a mouse neuroblastoma cells stably transfected with the hKOPR (N2A-3HA-hKOPR), U50,488H robustly induced neurite outgrowth, but etorphine caused outgrowth to a much lower extent. G protein-dependent pathway was found to be involved in the actions of both agonists, but β-arrestin-dependent pathway was not. Inhibition of ERK1/2 phosphorylation decreased neurite outgrowth promoted by both agonists, indicating the roles of MAP kinase cascades in KOPR agonist-induced neuritogenesis. In contrast, β-arrestin2, 14-3-3ζ, GEC1 and Rap1 are not involved in U50,488H- or etorphine-promoted neurite outgrowth. Thus, the two agonists appear to share the same signaling pathways and the difference between two agonists is likely due to the lower efficacy of etorphine. For the chapter 2, U50,488H caused phosphorylation of the mKOPR at S356, T357, T363 and S369 in N2A cells stably transfected with FmK6H (FmK6H-N2A cells). NorBNI abolished U50,488H-induced KOPR phosphorylation at all four residues. GRKs (GRKs2, 3, 5 and 6) and PKCs were involved in U50,488H-mediated KOPR phosphorylation. In addition, PKC also participated in agonist-independent KOPR phosphorylation. This is the first time that PKC was shown to be involved in agonist-induced KOPR phosphorylation. We found that U50,488H caused KOPR phosphorylation at T363 and S369 in the mouse brain and PKC participated in phosphorylation of S369, but not T363, by using the PKC inhibitor chelerythrine (CHL). Thus, we further characterized effects of PKC inhibition on KOPR-mediated behaviors in CD1 mice. PKC was involved in KOPR-mediated sedation, motor incoordination and conditioned place aversion, but not analgesia and anti-scratching effect in mice. Studies in this thesis revealed the mechanisms of KOPR-mediated neurite outgrowth and KOPR-mediated phosphorylation and the involvement of PKC in KOPR-mediated pharmacological effects in vivo. These studies push the frontier of molecular pharmacology of the KOPR, which may be useful for development of KOPR agonists for therapeutic use.
Temple University--Theses
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Dressano, Keini. "Interação do AtRALF1 com o receptor quinase1 associado ao BRI1 (BAK1)." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/11/11137/tde-26052015-164356/.

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Os peptídeos hormonais vegetais, que vêm sendo caracterizados em plantas desde a década de 90, podem estar relacionados com defesa, reprodução, crescimento e desenvolvimento de plantas. O peptídeo RALF (Rapid Alkalinization Factor), ubíquo no reino vegetal, está envolvido com o desenvolvimento de plantas. Em arabidopsis há 37 genes que codificam peptídeos RALF (AtRALFs). A isoforma mais estudada é a AtRALF1, a qual regula de maneira negativa a expansão celular, inibindo o crescimento de raiz primária e o alongamento de hipocótilo quando aplicado exogenamente. Recentemente, demonstrou-se a existência de uma relação antagônica entre AtRALF1 e a via de brassinosteróides (BRs) no desenvolvimento de raízes. Quando mutantes da via de sinalização do BR foram avaliados quanto a sua resposta ao peptídeo AtRALF1, descobriu-se que mutantes para o receptor quinase1 associado ao BRI1 (bak1) são insensíveis a AtRALF1. Experimentos utilizando o sistema de duplo híbrido em levedura, a co-imunoprecipitação e a indução de genes marcadores em mutantes bak1 foram realizados e confirmaram o envolvimento da proteína BAK1 na percepção do peptídeo. Plantas transgênicas que superexpressam AtRALF1 apresentam um fenótipo semi-anão, no entanto, quando as mesmas foram cruzadas com o mutante bak1, suas progênies apresentaram um fenótipo similar ao de plantas selvagens. Ainda, quando plantas deste cruzamento foram novamente cruzadas com plantas selvagens, plantas com fenótipo semi-anão foram observadas na prole. Ensaios de ligação usando o peptídeo AtRALF1 marcado com éster de acridínio foram realizados e mostraram que em mutantes bak1, a ligação do AtRALF1 é menor em aproximadamente 30% quando comparada com plantas selvagens. Os dados obtidos mostram que a proteína BAK1 interage fisicamente com o AtRALF1, está envolvida na percepção do peptídeo, é essencial para a inibição do crescimento da raiz primária causada pelo AtRALF1 e é necessária para a indução dos genes responsivos ao AtRALF1.
The plant peptides, which have been characterized in plants since the 90\'s, can be related to defense, reproduction, growth and development of plants. The RALF (Rapid Alkalinization Factor) peptide, ubiquitous in the plant kingdom, is related to the development of plants. In arabidopsis plants, there are 37 genes encoding RALF peptides (AtRALFs). AtRALF1 is the most studied isoform, which negatively regulate cell expansion, inhibiting primary root growth and hypocotyl elongation when it is applied exogenously. Recently, an antagonistic relationship between AtRALF1 and the brassinosteroids (BRs) to control root development had been demonstrated. When the response of mutants related to the BR signaling pathway to AtRALF1 peptide was investigated, it was found that mutants lacking the BRI1-associated receptor kinase1 (bak1) are insensitive to AtRALF1. Experiments using the two-hybrid system in yeast, co-immunoprecipitation, and the induction of marker genes in bak1 mutants were carried out, and confirmed the involvement of the BAK1 protein in the perception of AtRALF1 peptide. Transgenic plants overexpressing AtRALF1 are semi-dwarf. However, when those transgenic plants were crossed with bak1 mutant, their progeny showed a wild-type phenotype. Besides, when plants from this progeny were crossed again with wild-type plants, semi-dwarf phenotype plants were obtained in the offspring. Binding assays using AtRALF1 labeled with acridinium-ester were performed, and showed that in bak1 mutants, the AtRALF1 binding was reduced approximately 30% when compared to wild-type plants. All data indicate that BAK1 protein interacts physically with AtRALF1, it\'s involved with the peptide perception, essential for the primary root growth inhibition caused by AtRALF1, and required to the induction of genes responsive to AtRALF1.
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Fu, Hangfei. "Interleukin 35 inhibits ischemia-induced angiogenesis essentially through the key receptor subunit Interleukin 12 receptor beta 2." Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/546609.

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Biomedical Sciences
Ph.D.
Peripheral arterial disease (PAD) is a worldwide disease caused by atherosclerosis. It is a circulatory condition where narrowed blood vessels reduce blood flow to the peripheral such as legs. Although current gold standard treatment for advanced PAD patients is still based on surgical revascularization, there is no effective therapy for many patients that are not suitable for surgery. In addition, better recovery from surgical revascularization largely relies on angiogenesis in the adjacent ischemic tissue. Thus, novel pro-angiogenic therapies to improve post-ischemic neovascularization are urgently desired. However, current poor understanding of the roles of anti-inflammatory cytokines in angiogenesis prevents the development of these new therapies. We and others have reported that IL-35 is a newly identified inducible immunosuppressive heterodimeric cytokine in the IL-12 family. IL-35 is composed of p35 (IL-12A) and EBI3, and its receptors are comprised of homodimers or heterodimer of IL-12Rb2 and gp130 (IL-6ST). We have shown that IL-35 inhibits endothelial cell (EC) activation induced by lipopolysaccharide (LPS) or atherogenic lysophosphatidylcholine (LPC). At least partially through these new EC-dependent mechanisms, IL-35 inhibits inflammation in autoimmune diseases, infectious diseases, atherosclerosis, and tumors. Recent studies have indicated the role of IL-35 in angiogenesis in rheumatoid arthritis and different tumors. However, whether and how IL-35 regulates post-ischemic angiogenesis in peripheral artery disease are unrevealed. In our study, we used hindlimb ischemia (HLI) and Matrigel plug assay as in vivo angiogenesis models and wound healing assay as in vitro angiogenesis model to study the role and underlying mechanisms of IL-35-mediated angiogenesis. We made the following findings: 1) muscle in human and mouse has high angiogenic potential in physiological conditions; 2) angiogenic cytokines and chemokines including anti-inflammatory cytokines are predominantly regulated by inflammatory transcription factors; 3) IL-35 signaling is induced in ischemic muscle; 4) IL-12Rb2, but not IL-6ST, is the key receptor component of IL-35 signaling in ischemic muscle and hypoxic human microvascular endothelial cells (HMVECs); 5) hyperlipidemia (atherogenic factor) impairs angiogenesis in vivo and in vitro, which partially acts through the induction of IL-35; 6) IL-12Rb2 deficiency improves HLI-induced angiogenesis in both WT or apolipoprotein E (ApoE) -/- mice (an atherosclerosis model); 7) IL-35 injection inhibits HLI-induced angiogenesis in WT mice but not that in the IL-12Rb2 deficient mice; 8) IL-35 injection enlarges the avascular area in gastrocnemius muscle after HLI; 9) IL-35 obstructs fibroblast growth factor-2 (FGF2)-induced angiogenesis in Matrigel plug assay in vivo; 10) CD45-CD31+ ECs from the IL-35-injected ischemic muscle at day 14 of HLI have an abnormal extracellular matrix organization, activated integrin pathways (cell-matrix adhesions), disrupted vascular endothelial (VE)-cadherin-plakoglobin complex (cell-cell adhesions), and increased infiltration and migration of bone marrow-derived leukocytes; 11) IL-35 inhibits HMVEC migration in wound healing assay in vitro presumably through upregulation of anti-angiogenic proteins including pigment epithelium-derived factor (PEDF), serpin family B member 5 (SERPINB5, Maspin), and thrombospondin (THBS)-1. These results suggest that anti-inflammatory cytokine IL-35, signaling through the key receptor subunit IL-12Rb2, inhibits HLI-induced angiogenesis and delays tissue repair by dysregulating cell-cell and cell-matrix adhesions, which leads to the impaired vascular adhesion junction and maturation of blood vessels.
Temple University--Theses
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Bryan, Anthony C. "Social Networks of Receptor-like Kinases Regulate Cell Identity in Arabidopsis thaliana." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/205180.

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Receptor-like kinases (RLKs) make up one of the largest gene families in Arabidopsis thaliana. These genes are required for various biological processes, including response to biotic stress, cell elongation, cell proliferation, and cell fate patterning. An emerging theme in Arabidopsis and other plants is that networks of RLKs are required to regulate a specific process throughout development involving spatial and temporal regulation of transcription factors. However, there are still many RLKs (>50%) with no known function.Several RLKs regulate epidermal development by contributing to early embryonic epidermal maintenance or to epidermal differentiation. In my first analysis, I characterize the role of two related RLKs GASSHO1 (GSO1) and GSO2 in epidermal differentiation. gso1 gso2 double mutants initially form an epidermis during embryogenesis, but analysis of post-embryonic root development indicates the mis-expression of epidermal-specific genes. Three previously characterized RLKs that are involved in epidermal development are also involved in meristem maintenance. In order to decipher the RLK gene networks controlling epidermal development and meristem maintenance, it is necessary to identify additional RLKs involved in both of these processes. I further identified roles for GSO1 and GSO2 in maintaining root growth and root apical meristem (RAM) activity. A future goal will be to elucidate the networks of RLKs, including GSO1 and GSO2 in regulating epidermal and RAM development.The development of the vasculature in plants is controlled by a vascular meristem, the procambium. Oriented cell divisions from the procambium produce phloem, to the periphery, and xylem, to the center of the plant. In a reverse genetic screen to determine to roles of the remaining RLKs with unknown function, we identified the RLK XYLEM INTERMIXED WITH PHLOEM1 (XIP1) that is required for vascular development. We show XIP1 is required for regulating the differentiation of the phloem and for the organization of xylem vessel elements. Our analysis indicates that XIP1 is part of a vascular meristem network, further emphasizing the importance of social networks of RLKs regulating a specific process in development.
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Geider, Kirsten [Verfasser], Bodo [Akademischer Betreuer] Laube, and Ralf [Akademischer Betreuer] Galuske. "Ionotropic glutamate receptor dysfunction in pediatric neurodevelopment / Kirsten Geider. Betreuer: Bodo Laube ; Ralf Galuske." Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2015. http://d-nb.info/1110981228/34.

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Inan, Saadet. "Pharmacological and Neuroanatomical Analysis of GNTI-Induced Repetitive Behavior in Mice." Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/75332.

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Pharmacology
Ph.D.
This thesis is comprised of two parts. In the first part, we investigated a) the pharmacology of GNTI, a selective kappa opioid receptor antagonist, as a scratch-inducing compound in mice and b) possible mediators and receptors that may be involved in GNTI-induced scratching (itch). We studied if GNTI induces scratching through opioid, histamine, gastrin-releasing peptide (GRP) and/or muscarinic M1 receptors. In the second part, we established similarities and differences between pain and itch using GNTI-induced scratching and formalin-induced nociception models in mice. We found that GNTI (0.03-3 mg/kg, s.c., behind the neck) induces compulsive and vigorous scratching behavior in a dose-dependent manner. A standard submaximal dose (0.3 mg/kg) of GNTI caused animals to scratch 500-600 times in a 30 min observation period. Intrathecal (i.t.) or intraperitoneal (i.p.) administration of GNTI did not elicit scratching behavior. Duration of action of GNTI was 60-70 min and tolerance to the repetitive behavior did not develop. C-fos expressing neurons, in response to GNTI injection, were localized on the lateral side of the superficial layers of the dorsal horn of the cervical spinal cord. Compound 48/80, a chemically different pruritogen, evoked c-fos expression in neurons which are located on the lateral side of the superficial layer of the dorsal horn. These data suggest that both GNTI and compound 48/80 activate a group of sensory neurons located on the lateral side of lamina I and II. Pretreating (at -20 min) and posttreating (at +5 min) mice with the kappa opioid receptor agonist, nalfurafine (0.001-0.03 mg/kg, s.c.), significantly attenuated scratching induced by GNTI (0.3 mg/kg). These effects were not a consequence of behavioral depression. Tolerance did not develop to the anti-scratch activity of nalfurafine. Pretreating mice with nalfurafine (0.02 mg/kg) prevented both GNTI- and compound 48/80-provoked c-fos expression. Our c-fos results suggest that the preclinical antipruritic activity of nalfurafine occurs at the spinal level. Moreover, our results reinforce the need to evaluate nalfurafine as a potentially useful antipruritic in human conditions involving itch. GNTI still elicited excessive scratching in mice lacking mu, delta or kappa opioid receptors, respectively, as well as in mice pretreated with either naloxone or norbinaltorphimine. The H1 receptor antagonist, fexofenadine, or the H4 receptor antagonist, JNJ 10191584, did not attenuate GNTI-induced scratching. Also, pretreating mice with the peptide GRPR antagonist, [D-Phe6]bombesin(6-13) methyl ester, or the non-peptide GRPR antagonist, RC-3095, did not antagonize scratching induced by GNTI. Furthermore, GRPR mRNA levels did not change in response to GNTI injection. Telenzepine, a standard M1 receptor antagonist, had no marked effect against GNTI-elicited scratching, however (unexpectedly) McN-A-343, an M1 receptor agonist, attenuated this behavior in a dose-dependent manner. In the second part of our studies, we found that pretreating mice with lidocaine (i.d., behind the neck) inhibits GNTI-induced scratching and prevents GNTI-provoked c-fos expression in the dorsal horn of the spinal cord. Similarly, lidocaine (i.d., hind leg) inhibits formalin-induced nociception as well as formalin-provoked c-fos expression. While injection (s.c.) of formalin to the face of mice induced only wiping (indicating pain) by forepaws of the injection side, injection (s.c.) of GNTI to the face elicited grooming and scratching (indicating itch). In contrast to formalin, GNTI did not induce c-fos expression in the trigeminal nucleus suggesting that pain and itch sensations are projected differently along the sensory trigeminal pathway. In short, our main results indicate that a) the scratch-inducing activity of GNTI is not mediated by opioid, histamine or GRP receptors; b) kappa opioid receptors are involved, at least in part, in the inhibition of itch sensation and thus, on the basis of our results, nalfurafine holds promise as a potentially useful antipruritic in human conditions involving itch; and c) agonism at M1 receptors inhibits GNTI-induced scratching therefore the M1 receptor may be a key target for antipruritic drug development.
Temple University--Theses
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Books on the topic "RLF receptor"

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Ge, Zengxiang. Arabidopsis BUPS-ANX Receptor Complex Coordinates with RALF Peptides to Regulate Pollen Tube Integrity and Sperm Release. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5491-9.

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Ge, Zengxiang. Arabidopsis BUPS-ANX Receptor Complex Coordinates with RALF Peptides to Regulate Pollen Tube Integrity and Sperm Release. Springer, 2020.

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Ge, Zengxiang. Arabidopsis BUPS-ANX Receptor Complex Coordinates with RALF Peptides to Regulate Pollen Tube Integrity and Sperm Release. Springer, 2020.

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Hansen, Hendrik, and Tim Kraski Lic., eds. Politischer und wirtschaftlicher Liberalismus. Nomos Verlagsgesellschaft mbH & Co. KG, 2019. http://dx.doi.org/10.5771/9783845239286.

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The metaphor of the ‘invisible hand’ not only characterises Smith’s understanding of competitive processes in free markets but also his theory of political liberalism. Smithʼs theory of economic and political liberalism is based on the assumption of autonomous processes in the development of morality, laws and the social order. These processes lead to a natural harmony of individual interests in politics and economics. However, Smith does not associate these ideas with the demand for a minimal state. Instead, he assigns the state a much more active role than is generally assumed. The analyses in this book of Smith’s reception by authors in the 19th century (in the US and Germany) and of his relevance for current analyses of political challenges show that the question of which conditions need to be fulfilled to ensure the stability of liberal societies is still a crucial one in political philosophy and science. With contributions by Michael Aßländer, Christel Fricke, Hendrik Hansen, Michael Hochgeschwender, Tobias Knobloch, Tim Kraski, Heinz D. Kurz, Birger Priddat, Bastian Ronge, Rolf Steltemeier, Richard Sturn
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Endreß, Alexander, and Hubert Wandjo, eds. Musikwirtschaft im Zeitalter der Digitalisierung. Nomos Verlagsgesellschaft mbH & Co. KG, 2021. http://dx.doi.org/10.5771/9783845276939.

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How does one deal with the digitalisation of an industry when practice is overtaking itself so quickly, as the music industry has experienced in the past twenty years? On the one hand, by questioning the causes of change and, on the other hand, by describing and reflecting on practice. Both are done in this book. The music industry is understood as a complex system based on the division of labour, in which artist development, content production, content marketing and rights management go hand in hand. Special attention is therefore paid to these operative fields of action. The practice-oriented explanations are complemented by a description of the normative and cultural framework conditions to which the music production, distribution and reception system is subject. The articles are written by music industry experts from academia and practice and focus in particular on digital competencies and industry structures. In this respect, this book is not only interesting for (future) professionals in the music and creative industries. Academics can also benefit from these practical reports and future theses on the digital transformation of the music industry. With contributions by Christian Baierle, Sophie Brüggemann, Florian Drücke, Alexander Endreß, Frank Fenslau, Hanno Fierdag, Jörg Fukking, Dirk Geibel, Steffen Geldner, René Houareau, Lucas Holczinger, Ralf Kitzberger, Peter Knees, David Maier, Armin Oldendorf, Matthias Rauch, Ryan Rauscher, Tim Renner, Markus Rennhack, Julien Schaffhauser, Nina Schneider, Stefan Schulte-Holthaus, Jeong-Won Sin, Kolja Spohn, Nina Christin Stehr, Peter Tschmuck, Hubert Wandjo, Heiko Wandler, Stefan Weinacht, Asterix David Westphal, Peter Wicke and David-Emil Wickström.
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Book chapters on the topic "RLF receptor"

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Brustolini, Otávio J. B., José Cleydson F. Silva, Tetsu Sakamoto, and Elizabeth P. B. Fontes. "Bioinformatics Analysis of the Receptor-Like Kinase (RLK) Superfamily." In Methods in Molecular Biology, 123–32. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6859-6_9.

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Mage, Rose G., and Claire Rogel-Gaillard. "Immunogenetics in the rabbit." In The genetics and genomics of the rabbit, 66–83. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781780643342.0005.

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Abstract This chapter on immunogenetics in the rabbit focused on some genes with genetic and genomic sequence information including those encoding: soluble circulating immunoglobulin molecules (Igs) and their surface-bound forms on B lymphocytes (BCRs); T-cell receptors on T lymphocyte surfaces, (TCRs); the rabbit Leukocyte Antigen (RLA) complex (proteins on cells that function to present antigen fragments to TCRs); and some cytokine genes that encode key regulators of T- and B-cell responses.
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Cai, Jun, and Yanda Li. "Classification of Nuclear Receptor Subfamilies with RBF Kernel in Support Vector Machine." In Advances in Neural Networks – ISNN 2005, 680–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11427469_108.

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Ge, Zengxiang. "Receptor-Like Kinases BUPS1/2 are Involved in Pollen Tubes Integrity Maintenance in Arabidopsis." In Arabidopsis BUPS-ANX Receptor Complex Coordinates with RALF Peptides to Regulate Pollen Tube Integrity and Sperm Release, 15–36. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5491-9_2.

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Ge, Zengxiang. "Review of Cell–Cell Communication in Plant Reproduction." In Arabidopsis BUPS-ANX Receptor Complex Coordinates with RALF Peptides to Regulate Pollen Tube Integrity and Sperm Release, 1–13. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5491-9_1.

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Ge, Zengxiang. "RALF4/19 are Autocrine Signals to Maintain Pollen Tubes Integrity." In Arabidopsis BUPS-ANX Receptor Complex Coordinates with RALF Peptides to Regulate Pollen Tube Integrity and Sperm Release, 37–57. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5491-9_3.

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Ge, Zengxiang. "RALF34 is a Paracrine Signal to Trigger Pollen Tubes Burst and Sperm Release." In Arabidopsis BUPS-ANX Receptor Complex Coordinates with RALF Peptides to Regulate Pollen Tube Integrity and Sperm Release, 59–71. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5491-9_4.

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Rougé, Pierre, Wim Nerinckx, Clare Gough, Jean-Jacques Bono, and Annick Barre. "Docking of Chitin Oligomers and Nod Factors on Lectin Domains of the LysM-RLK Receptors in the Medicago-Rhizobium Symbiosis." In Advances in Experimental Medicine and Biology, 511–21. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7877-6_27.

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Evans Adunyah, Samuel, Richard Akomeah, Fareed K.N. Arthur, Roland S. Cooper, and Joshua C.M. Williams. "IL-17 Biological Effects and Signaling Mechanisms in Human Leukemia U937 Cells." In Interleukins - The Immune and Non-Immune Systems’ Related Cytokines. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96422.

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Human Interlekin-17 is produced by memory activated CD4+ T cells and other cells. It was initially considered unique in that its specific receptor is distinct from other cytokine receptors. IL-17 receptor is ubiquitously expressed by different cells including T cells. IL-17 plays a role in regulating growth, immune response and pro-inflammatory responses. It regulates differentiation of a subset of Th0 cells into Th-17 cells, which produce IL-17-induced cytokines. The IL-17R belongs to type 1 cytokine receptors. IL-17 belongs to a superfamily of its own, which includes IL-17A, IL-17B, IL-17C, IL-17E and IL-17F. These members of IL-17 superfamily have some sequence homology but bind to different receptors. Prior to this investigation, limited information existed on the effects of IL-17A in human leukemia cell lines. Our results show that IL-17A promotes growth, anti-apoptotic effects, chemotaxis, cytokine expression and transcriptional factor activation in leukemia cells. IL-17A activates multiple signaling pathways including PI-3 K, Jak–STAT, Raf-ERK1/2 and SRC kinase pathways, which mediate different biological effects of IL-17A in leukemia cells. Our findings implicate IL-17A in leukemia cell growth and survival, supporting potential leukemia therapy via development of anti-IL-17A drugs. This chapter focuses on IL-17A, herein referred to as IL-17.
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Casoni, Francesca, Andrea Galbiati, and Luigi Ferini-Strambi. "D3 receptor agonist efficacy in restless legs syndrome." In Pharmacology of Restless Legs Syndrome (RLS), 21–35. Elsevier, 2019. http://dx.doi.org/10.1016/bs.apha.2019.01.005.

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Conference papers on the topic "RLF receptor"

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Hong, Seung-Keun. "Abstract 1938: Raf/MEK/ERK-mediated differential regulation of androgen receptor levels in prostate cancer cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1938.

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Teodorovic, Lenka S., Jacqueline Carrico, Deborah DeRyckere, Weihe Zhang, Xiaodong Wang, Stephen Frye, S. Gail Eckhardt, H. Shelton Earp, and Douglas K. Graham. "Abstract 730: Efficacy of a novel small molecule MER receptor tyrosine kinase inhibitor in B-RAF wild-type and B-RAF mutant melanoma cell lines." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-730.

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Mishra, Prashant Kumar, D. R. Jahagirdar, and Girish Kumar. "Circularly polarized active antenna array for telemetry reception." In 2014 IEEE International Microwave and RF Conference (IMaRC). IEEE, 2014. http://dx.doi.org/10.1109/imarc.2014.7039028.

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Torrecilla Patiño, Elia, and Miguel Molina Alarcón. "Performances mínimas en el espacio urbano y colaboraciones a distancia. Propuestas de “Acciones Desapercibidas” como experiencia entre lo local y lo translocal." In III Congreso Internacional de Investigación en Artes Visuales :: ANIAV 2017 :: GLOCAL. Valencia: Universitat Politècnica València, 2017. http://dx.doi.org/10.4995/aniav.2017.4899.

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En la presente comunicación mostramos la experiencia obtenida de la participación en un proyecto internacional y su puesta en acción en el ámbito local. Partiendo de la investigación sobre cuestiones que abordan la relación entre cuerpo, ciudad y tecnología, comenzamos a experimentar en el espacio urbano la práctica de una serie de performances mínimas inscritas en el ámbito de lo cotidiano. Tras el descubrimiento de una propuesta desarrollada en Holanda, profundizamos en el uso de la ciudad como laboratorio y escenario donde llevar a cabo nuestras Acciones Desapercibidas; así comenzamos una serie de colaboraciones con los organizadores del Unnoticed Art Festival de Holanda, empleando, en ocasiones, el uso de dispositivos móviles. Este es el caso de Parallel Walks, una serie de paseos paralelos simultáneos en los que deambulamos siguiendo las directrices que nos enviamos, de una ciudad a otra a través de mensajería instantánea, creando un recorrido en una tercera ciudad resultante de ambas. De este modo, las prácticas artísticas colectivas se vuelven más accesibles y nos permiten experimentar nuevas posibilidades que incluyen las colaboraciones a distancia, la translocalización, la simultaneidad y la posibilidad de realizar acciones y desplazarnos por una ciudad híbrida.Finalmente, llevamos esta experiencia al ámbito de la docencia realizando acciones mínimas en el espacio urbano de Valencia, con propuestas creadas por los propios estudiantes, junto a otras que restituían algunos referentes de arte de acción del periodo de la vanguardia histórica española. Esta parte de recuperación histórica, se realizó con el fin de utilizar el cuerpo como generador de historia desde la investigación-acción y comprobar si su recepción actual sería la misma o no, así como jugar y producir nuevas relecturas entre presente-pasado, local-global, creador-receptor, Arte-NoArte o cotidianidad-sorpresa. Estos resultados forman parte de un proyecto I+D concedido por el Ministerio de Economía y Competitividad (ref. HAR2014-58869-P).http://dx.doi.org/10.4995/ANIAV.2017.4899
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Maxim, A., C. Turinici, and M. Gheorge. "Antenna Diversity Zero-Second-IF SiGe BiCMOS Satellite Radio Tuner for Deep Fading Automotive Mobile Reception." In 2008 IEEE Topical Meeting on Silicon Monolithic Integrated Circuits in RF Systems. IEEE, 2008. http://dx.doi.org/10.1109/smic.2007.7.

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Ray, Jayanta Kumar, Abhipray Singh, Quazi Md Alfred, Subhankar Shome, and Rabindranath Bera. "5G URLLC Communication System With Cognitive Radio and Frequency Diversity Reception For Improving Reliability In Smart Factory E-cranes operation." In 2019 IEEE MTT-S International Microwave and RF Conference (IMARC). IEEE, 2019. http://dx.doi.org/10.1109/imarc45935.2019.9118760.

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Maxim, A., C. Turinici, and M. Gheorge. "Notice of Violation of IEEE Publication Principles: Antenna Diversity Zero-Second-IF SiGe BiCMOS Satellite Radio Tuner for Deep Fading Automotive Mobile Reception." In 2008 IEEE Topical Meeting on Silicon Monolithic Integrated Circuits in RF Systems. IEEE, 2008. http://dx.doi.org/10.1109/smic.2008.7.

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Krasnoshtanova, Alla, and Alesya Yudina. "PRODUCTION OF ANTIBODIES FROM POULTRY YOLK (IgY) AND INVESTIGATION OF THEIR IMMUNOCHEMICAL PROPERTIES." In GEOLINKS Conference Proceedings. Saima Consult Ltd, 2021. http://dx.doi.org/10.32008/geolinks2021/b1/v3/17.

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"A particularly important aspect of immunology is to develop non-invasive methods of obtaining antibodies which could be a great alternative to traditional ones that based on the harmful procedure of isolation of immunoglobulins from animal blood sera. That’s why the extraction of antibodies from poultry egg yolks (IgY) is the most promising. Due to the fact of variation of IgY structural features that determine the definite immunochemical properties, yolk antibodies in comparison with mammalian immunoglobulins (IgG) does not interact with rheumatoid factor (Rf), contribute to the activation of the complement system, bind to the Fc-receptor (FcR), and also has weak cross-reactivity, which confirms the possibility of their widespread use in medicine and food. Also the presence of phylogenetic distance between chickens and mammalians guarantees immune response against conservative mammalian protein molecules which is highly important for the creation of new generation test systems. The aim of this work is to develop a selective method of producing high-purity immunoglobulin Y preparations from the yolk of chicken eggs. There were adopted selective conditions of isolation of IgY under spontaneous thawing procedure at the room temperature of firstly frozen yolk solution in a sodium-phosphate buffer mixed with water (pH 5.0) in a ratio of 1:6, which leads to receiving a water-soluble fraction further precipitated with the sodium chloride at a concentration of 10% of the solution mass and subsequently concentrated using ultrafiltration with membrane UAM-10, that allows achieving the content of IgY not less than 95% per dry substance in immunoglobulin fraction. It is possible to produce a protein fraction with a protein content of at least 9 g/l. The purity of the immunoglobulin fraction was verified using polyacrylamide gel electrophoresis. The presence of a light chain in the IgY solution was proved to be a low-molecular compound using the method of gel-filtration-chromatography. The immunological activity of IgY was studied with respect to bovine serum albumin (BSA) as an antigen. The enzymatic resistance of IgY against proteolytic enzymes was tested in area of the gastrointestinal tract."
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Su, Chin Cheng. "Abstract 2131: Tanshinone IIA can decrease growth factor receptors expression and dural-block both Ras/Raf/MEK/ERK and Ras/PI3K/Akt/mTOR pathways to inhibit human breast cancer BT-20 cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2131.

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Reports on the topic "RLF receptor"

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Idakwo, Gabriel, Sundar Thangapandian, Joseph Luttrell, Zhaoxian Zhou, Chaoyang Zhang, and Ping Gong. Deep learning-based structure-activity relationship modeling for multi-category toxicity classification : a case study of 10K Tox21 chemicals with high-throughput cell-based androgen receptor bioassay data. Engineer Research and Development Center (U.S.), July 2021. http://dx.doi.org/10.21079/11681/41302.

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Deep learning (DL) has attracted the attention of computational toxicologists as it offers a potentially greater power for in silico predictive toxicology than existing shallow learning algorithms. However, contradicting reports have been documented. To further explore the advantages of DL over shallow learning, we conducted this case study using two cell-based androgen receptor (AR) activity datasets with 10K chemicals generated from the Tox21 program. A nested double-loop cross-validation approach was adopted along with a stratified sampling strategy for partitioning chemicals of multiple AR activity classes (i.e., agonist, antagonist, inactive, and inconclusive) at the same distribution rates amongst the training, validation and test subsets. Deep neural networks (DNN) and random forest (RF), representing deep and shallow learning algorithms, respectively, were chosen to carry out structure-activity relationship-based chemical toxicity prediction. Results suggest that DNN significantly outperformed RF (p < 0.001, ANOVA) by 22–27% for four metrics (precision, recall, F-measure, and AUPRC) and by 11% for another (AUROC). Further in-depth analyses of chemical scaffolding shed insights on structural alerts for AR agonists/antagonists and inactive/inconclusive compounds, which may aid in future drug discovery and improvement of toxicity prediction modeling.
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