Relevant bibliographies by topics / NO receptor

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'NO receptor'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "NO receptor"

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Mangal, Suruchi, Manisha Sharma, Mridu Manjari, Rahul Mannan, and Sunit Tandon. "Expression Of Androgen Receptor, Estrogen Receptor And Progesterone Receptor In Endometrial Carcinoma (Immunohistochemical Study)." Annals of Pathology and Laboratory Medicine 7, no. 5 (May 28, 2020): A248–252. http://dx.doi.org/10.21276/apalm.2726.

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Johnstone, Elizabeth K. M., and Kevin D. G. Pfleger. "Profiling novel pharmacology of receptor complexes using Receptor-HIT." Biochemical Society Transactions 49, no. 4 (August 26, 2021): 1555–65. http://dx.doi.org/10.1042/bst20201110.

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Many receptors are able to undergo heteromerisation, leading to the formation of receptor complexes that may have pharmacological profiles distinct from those of the individual receptors. As a consequence of this, receptor heteromers can be classed as new drug targets, with the potential for achieving greater specificity and selectivity over targeting their constituent receptors. We have developed the Receptor-Heteromer Investigation Technology (Receptor-HIT), which enables the detection of receptor heteromers using a proximity-based reporter system such as bioluminescence resonance energy transfer (BRET). Receptor-HIT detects heteromers in live cells and in real time, by utilising ligand-induced signals that arise from altered interactions with specific biomolecules, such as ligands or proteins. Furthermore, monitoring the interaction between the receptors and the specific biomolecules generates functional information about the heteromer that can be pharmacologically quantified. This review will discuss various applications of Receptor-HIT, including its use with different classes of receptors (e.g. G protein-coupled receptors (GPCRs), receptor tyrosine kinases (RTKs) and others), its use to monitor receptor interactions both intracellularly and extracellularly, and also its use with genome-edited endogenous proteins.
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Nieber, Karen, and Sebastian Michael. "Adenosine receptors: Intermembrane receptor–receptor interactions in the brain." Synergy 1, no. 2 (December 2014): 83–91. http://dx.doi.org/10.1016/j.synres.2014.10.001.

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Ecke, Denise, Theodor Hanck, Mohan E. Tulapurkar, Rainer Schäfer, Matthias Kassack, Rolf Stricker, and Georg Reiser. "Hetero-oligomerization of the P2Y11 receptor with the P2Y1 receptor controls the internalization and ligand selectivity of the P2Y11 receptor." Biochemical Journal 409, no. 1 (December 11, 2007): 107–16. http://dx.doi.org/10.1042/bj20070671.

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Nucleotides signal through purinergic receptors such as the P2 receptors, which are subdivided into the ionotropic P2X receptors and the metabotropic P2Y receptors. The diversity of functions within the purinergic receptor family is required for the tissue-specificity of nucleotide signalling. In the present study, hetero-oligomerization between two metabotropic P2Y receptor subtypes is established. These receptors, P2Y1 and P2Y11, were found to associate together when co-expressed in HEK293 cells. This association was detected by co-pull-down, immunoprecipitation and FRET (fluorescence resonance energy transfer) experiments. We found a striking functional consequence of the interaction between the P2Y11 receptor and the P2Y1 receptor where this interaction promotes agonist-induced internalization of the P2Y11 receptor. This is remarkable because the P2Y11 receptor by itself is not able to undergo endocytosis. Co-internalization of these receptors was also seen in 1321N1 astrocytoma cells co-expressing both P2Y11 and P2Y1 receptors, upon stimulation with ATP or the P2Y1 receptor-specific agonist 2-MeS-ADP. 1321N1 astrocytoma cells do not express endogenous P2Y receptors. Moreover, in HEK293 cells, the P2Y11 receptor was found to functionally associate with endogenous P2Y1 receptors. Treatment of HEK293 cells with siRNA (small interfering RNA) directed against the P2Y1 receptor diminished the agonist-induced endocytosis of the heterologously expressed GFP–P2Y11 receptor. Pharmacological characteristics of the P2Y11 receptor expressed in HEK293 cells were determined by recording Ca2+ responses after nucleotide stimulation. This analysis revealed a ligand specificity which was different from the agonist profile established in cells expressing the P2Y11 receptor as the only metabotropic nucleotide receptor. Thus the hetero-oligomerization of the P2Y1 and P2Y11 receptors allows novel functions of the P2Y11 receptor in response to extracellular nucleotides.
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Doukhanina, Elena V., Nestor R. Apuya, Hye-Dong Yoo, Chuan-Yin Wu, Patricia Davidow, Shannon Krueger, Richard B. Flavell, Richard Hamilton, and Steven C. Bobzin. "Expression of Human Nuclear Receptors in Plants for the Discovery of Plant-Derived Ligands." Journal of Biomolecular Screening 12, no. 3 (January 26, 2007): 385–95. http://dx.doi.org/10.1177/1087057107299255.

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Plants have the potential to produce a wide array of secondary metabolites that have utility as drugs to treat human diseases. To tap this potential, functional human nuclear receptors have been expressed in plants to create in planta screening assays as a tool to discover natural product ligands. Assays have been designed and validated using 3 nuclear receptors: the estrogen receptor (ER), the androgen receptor (AR), and the heterodimeric retinoid X receptor-α plus thyroid hormone receptorβ (RXRA/THRB). Nuclear receptor—reporter constructs have been expressed in plants to detect the presence of natural ligands that are produced de novo in several plant species during different stages of development, in various tissues, and in response to different stress elicitors. Screening experiments with ER, AR, and RXRA/THRB have been conducted, leading to the identification of plant sources of natural product ligands of human nuclear receptors. This in planta screen has led to the identification of previously unreported ER ligands, providing evidence of the complementary value of this approach to current in vitro high-throughput screening assays. ( Journal of Biomolecular Screening 2007:385-395)
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Presky, D. H., U. Gubler, R. A. Chizzonite, and M. K. Gately. "IL12 receptors and receptor antagonists." Research in Immunology 146, no. 7-8 (September 1995): 439–45. http://dx.doi.org/10.1016/0923-2494(96)83013-6.

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Hu, Wenhui, Sunila Mahavadi, Jiean Huang, Fang Li, and Karnam S. Murthy. "Characterization of S1P1 and S1P2 receptor function in smooth muscle by receptor silencing and receptor protection." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 4 (October 2006): G605—G610. http://dx.doi.org/10.1152/ajpgi.00147.2006.

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Sphingosine-1-phosphate (S1P) induces an initial Ca2+-dependent contraction followed by a sustained Ca2+-independent, RhoA-mediated contraction in rabbit gastric smooth muscle cells. The cells coexpress S1P1 and S1P2 receptors, but the signaling pathways initiated by each receptor type and the involvement of one or both receptors in contraction are not known. Lentiviral vectors encoding small interfering RNAs were transiently transfected into cultured smooth muscle cells to silence S1P1 or S1P2 receptors. Phospholipase C (PLC)-β activity and Rho kinase activity were used as markers of pathways mediating initial and sustained contraction, respectively. Silencing of S1P1 receptors abolished S1P-stimulated activation of Gαi3 and partially inhibited activation of Gαi1, whereas silencing of S1P2 receptors abolished activation of Gαq, Gα13, and Gαi2 and partially inhibited activation of Gαi1. Silencing of S1P2 but not S1P1 receptors suppressed S1P-stimulated PLC-β and Rho kinase activities, implying that both signaling pathways were mediated by S1P2 receptors. The results obtained by receptor silencing were corroborated by receptor inactivation. The selective S1P1 receptor agonist SEW2871 did not stimulate PLC-β or Rho kinase activity or induce initial and sustained contraction; when this agonist was used to protect S1P1 receptors so as to enable chemical inactivation of S1P2 receptors, S1P did not elicit contraction, confirming that initial and sustained contraction was mediated by S1P2 receptors. Thus S1P1 and S1P2 receptors are coupled to distinct complements of G proteins. Only S1P2 receptors activate PLC-β and Rho kinase and mediate initial and sustained contraction.
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Mika, Kaan, Steeve Cruchet, Phing Chian Chai, Lucia L. Prieto-Godino, Thomas O. Auer, Sylvain Pradervand, and Richard Benton. "Olfactory receptor–dependent receptor repression in Drosophila." Science Advances 7, no. 32 (August 2021): eabe3745. http://dx.doi.org/10.1126/sciadv.abe3745.

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In olfactory systems across phyla, most sensory neurons express a single olfactory receptor gene selected from a large genomic repertoire. We describe previously unknown receptor gene–dependent mechanisms that ensure singular expression of receptors encoded by a tandem gene array [Ionotropic receptor 75c (Ir75c), Ir75b, and Ir75a, organized 5′ to 3′] in Drosophila melanogaster. Transcription from upstream genes in the cluster runs through the coding region of downstream loci and inhibits their expression in cis, most likely via transcriptional interference. Moreover, Ir75c blocks accumulation of other receptor proteins in trans through a protein-dependent, posttranscriptional mechanism. These repression mechanisms operate in endogenous neurons, in conjunction with cell type–specific gene regulatory networks, to ensure unique receptor expression. Our data provide evidence for inter-olfactory receptor regulation in invertebrates and highlight unprecedented, but potentially widespread, mechanisms for ensuring exclusive expression of chemosensory receptors, and other protein families, encoded by tandemly arranged genes.
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Arellano-Saab, Amir, Michael Bunsick, Hasan Al Galib, Wenda Zhao, Stefan Schuetz, James Michael Bradley, Zhenhua Xu, et al. "Three mutations repurpose a plant karrikin receptor to a strigolactone receptor." Proceedings of the National Academy of Sciences 118, no. 30 (July 23, 2021): e2103175118. http://dx.doi.org/10.1073/pnas.2103175118.

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Uncovering the basis of small-molecule hormone receptors’ evolution is paramount to a complete understanding of how protein structure drives function. In plants, hormone receptors for strigolactones are well suited to evolutionary inquiries because closely related homologs have different ligand preferences. More importantly, because of facile plant transgenic systems, receptors can be swapped and quickly assessed functionally in vivo. Here, we show that only three mutations are required to turn the nonstrigolactone receptor, KAI2, into a receptor that recognizes the plant hormone strigolactone. This modified receptor still retains its native function to perceive KAI2 ligands. Our directed evolution studies indicate that only a few keystone mutations are required to increase receptor promiscuity of KAI2, which may have implications for strigolactone receptor evolution in parasitic plants.
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De Weerth, A., J. R. Pisegna, and S. A. Wank. "Guinea pig gallbladder and pancreas possess identical CCK-A receptor subtypes: receptor cloning and expression." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 6 (December 1, 1993): G1116—G1121. http://dx.doi.org/10.1152/ajpgi.1993.265.6.g1116.

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Cholecystokinin (CCK) receptors mediate pancreatic acinar secretion and gallbladder contraction. Pharmacological and functional studies in pancreas and gallbladder demonstrate a CCK-A receptor subtype in both tissues. However, some pharmacological studies and affinity cross-linking studies of CCK receptors on pancreatic acini and gallbladder suggest that these two tissues possess two different subtypes of the CCK-A receptor. We cloned these receptors in guinea pig using a cDNA clone of the CCK-A receptor from rat pancreas. The guinea pig gallbladder CCK-A receptor was cloned by hybridization screening of a gallbladder cDNA library using a cDNA probe from the rat CCK-A receptor coding region. The guinea pig pancreas CCK-A receptor cDNA was cloned via the polymerase chain reaction using primers corresponding to the guinea pig gallbladder CCK-A receptor 5'- and 3'-noncoding regions. CCK-A receptor clones from guinea pig pancreas and gallbladder had identical nucleotide sequences, which were 80% homologous to the rat CCK-A receptor cDNA sequence. The deduced amino acid sequence from guinea pig CCK-A receptors was 89% homologous to the rat CCK-A receptor sequence. Dose-inhibition binding studies of transiently expressed receptors by CCK agonists and antagonists exhibited a CCK-A receptor pharmacologically similar to the rat CCK-A receptor. These studies indicate that the CCK-A receptors in guinea pig pancreas and gallbladder are identical and do not support previous proposals that they may represent different receptor subtypes.
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Dissertations / Theses on the topic "NO receptor"

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Ott, Thomas Ruthard. "Receptor activation in GNRH receptors." Doctoral thesis, University of Cape Town, 2000. http://hdl.handle.net/11427/2700.

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ZHANG, SHENGWEN. "THE OPIOID RECEPTOR-LIKE RECEPTOR ORL1: SIGNALING AND INTERACTION WITH OPIOID RECEPTORS." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1029419843.

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Zhang, Shengwen. "The opioid receptor-like receptor ORL1 signaling and interaction with opioid receptors /." Cincinnati, Ohio : University of Cincinnati, 2002. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1029419843.

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Oliveira-Giacomelli, Ágatha. "Papel dos receptores purinérgicos em modelo animal de doença de Parkinson." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-26112018-074709/.

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A Doença de Parkinson é uma doença altamente incapacitante e de grande prevalência. Pouco se sabe sobre sua etiologia e os tratamentos atuais consistem na diminuição dos sintomas, uma vez que ainda não foi encontrada uma maneira de reverter o déficit de neurônios dopaminérgicos observados nos pacientes acometidos. Sabe-se que os receptores purinérgicos são encontrados por todo o sistema nervoso central, não só no indivíduo adulto como também em diferentes estágios do desenvolvimento embrionário e estão envolvidos com proliferação e diferenciação celular. Este trabalho estudou a participação dos receptores purinérgicos em modelo animal de doença de Parkinson por lesão dos neurônios dopaminérgicos da via nigroestriatal com 6-OH dopamina (6-OHDA). Realizamos a análise do perfil de expressão gênica dos diferentes receptores após a lesão e subsequente modulação. Observamos expressão gênica alterada dos receptores P2X7 e P2Y6 até 5 semanas após a lesão. O uso do antagonista do receptor P2X7 Brilliant Blue G (BBG) induziu a regeneração da via nigroestriatal e o uso do antagonista do receptor P2Y6 MRS2578 preveniu a morte dos neurônios. Como esses efeitos foram acompanhados pela inativação de células microgliais, supõe-se que o controle do microambiente neuroinflamatório causado pela injeção de 6-OHDA seja a principal causa do efeito antiparkinsoniano observado pelo tratamento com BBG e MRS2578. Além disso, o transplante celular com células precursoras neuraisnão foi capaz de reverter o comportamento hemiparkinsoniano dos animais lesionados. Apesar do uso concomitante com BBG reduzir o comportamento, parece que esse efeito deve-se ao BBG per se, uma vez que o tratamento somente com o antagonista de P2X7 foi mais eficaz. De maneira geral, a modulação da atividade dos receptores purinérgicos se mostrou uma ferramenta promissora na pesquisa de cura e compreensão das bases moleculares da Doença de Parkinson
Parkinson\'s disease is a highly disabling and prevalent disease. Little is known about its etiology and the current treatments consist in the reduction of the symptoms, since there is no known method to reverse the dopaminergic neurons deficit observed in patients. Purinergic receptors are found throughout the central nervous system, not only in the adult individual but also at different stages of embryonic development, and are involved in proliferation and differentiation. This work investigated the role of purinergic receptors in the animal model of Parkinson\'s disease induced by 6-OH dopamine (6-OHDA) injection and consequent death of dopaminergic neurons of the nigrostriatal pathway. Patterns of purinergic receptors gene expression after the lesion and subsequent modulation were analyzed. We observed altered gene expression of P2X7 and P2Y6 receptors within 5 weeks of injury. The use of the P2X7 receptor antagonist Brilliant Blue G (BBG) induced the regeneration of the nigrostriatal pathway and treatment with P2Y6 receptor antagonist MRS2578 prevented the death of the neurons. Since these effects were accompanied by the inactivation of microglial cells, it is assumed that the control of neuroinflammatory milieu caused by the 6-OHDA injection is the main cause of the antiparkinsonian effect observed by the treatment with BBG and MRS2578. In addition, transplantation with neural precursor cells was not able to reverse the hemiparkinsonian behavior of injured animals. Although concomitant use with BBG improved cell engraftment, it appears that this effect is due to BBG per se, since treatment with only this P2X7receptor antagonist was more effective. In general, modulation of purinergic receptor activity showed to be a promising tool in the research of cure and understanding of the molecular bases of Parkinson\'s Disease.
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Sokolovski, Alexandra. "Sigma-1 Receptors Modulate NMDA Receptor Function." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23652.

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The sigma-1 receptor (σ-1R) is an endoplasmic reticulum (ER) protein that modulates a number of ion channels. It is hypothesized that σ-1Rs activated with agonist translocate to the plasma membrane. The σ-1R potentiates N-methyl-D-aspartate Receptors (NMDARs), important constituents of synaptic plasticity. NMDARs are anchored in the plasma membrane by Postsynaptic Density Protein-95 (PSD-95). The mechanism behind σ-1R modulation of NMDARs is not known. The results of my investigation confirm that σ-1Rs localize extrasomatically. Following σ-1R activation, σ-1R localization to dendrites and postsynaptic densities (PSDs) is upregulated. Unpublished work from our lab has shown that σ-1Rs associate with PSD-95 and NMDARs. Furthermore, immunocytochemistry (ICC) showed σ-1R colocalization with PSD-95 and NMDAR subunits. After σ-1R activation there was significantly increased colocalization between σ-1R, PSD-95, and GluN2B. Overall, this study may have provided insight into the molecular mechanism behind σ-1R modulation of NMDARs, which could have implications in the understanding of synaptic plasticity.
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Chakraborty, Raja. "Structure function studies on prostanoid receptors: Thromboxane A2 receptor (TP) and Prostacyclin receptor (IP)." Elsevier Ltd, 2011. http://hdl.handle.net/1993/23744.

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Cell membrane receptors help to mediate communication between the cell and its environment. The largest group of these membrane receptors belong to the family of G protein-coupled receptors (GPCRs). GPCRs contain seven transmembrane (TM) helices and signal predominantly through heterotrimeric G proteins in response to diverse extracellular stimuli. Previously, three levels of amino acid conservation were proposed to understand the structure and function of a GPCR. This includes “signature” amino acids, “group –conserved” amino acids and amino acids conserved only within a specific subfamily. The group-conserved residues in class A GPCR family involve amino acid conservation of up to 99% when considered as a group of small and weakly polar residues (Ala, Gly, Ser, Cys and Thr). These group-conserved residues have been proposed as key determinants in helix-helix interactions. Therefore, I selected these residues for structure-function analysis in the amine and the prostanoid receptor sub-families of class A GPCRs. Molecular and biochemical assays clearly demonstrate the importance of group-conserved residues in β2-adrenergic receptor and thromboxane A2 receptor (TP) structure and function. These studies led to the identification of a non-synonymous single nucleotide polymorphic variant (nsSNP) A160T in TP to be a constitutively active mutant (CAM). Further, the TP-CAM was used as a pharmacological tool that enabled classification of well-known TP-blockers, into neutral antagonists and inverse agonists. The role of TP-A160T in prostanoid receptors, TP- Prostacyclin receptor (IP) heterodimerization and signaling was investigated. Activation of a GPCR ultimately leads to structural changes in its intracellular loops (ICLs), which in turn activates G-protein. TP activates its cognate G protein (Gαq), while IP mediates signaling, through Gαs. Using TP-IP chimeric receptors, molecular modelling, and site directed mutagenesis studies I determined the specific ICL regions required for G protein coupling in TP and IP. Significant challenges exist in expressing and purifying GPCR-CAMs in amounts required to pursue biophysical studies. Using tetracycline inducible HEK293S system, A160T was expressed at high-levels and CD spectropolarimetry studies were successfully pursued on the purified A160T. The CD spectra showed that the loss of thermal stability of the A160T mutant is due to the subtle changes in the secondary structure of the A160T protein. These studies involving molecular, biochemical and pharmacological approaches provide novel insights into the structure and function of prostanoid receptors TP and IP.
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Jiang, Ning. "Kinetic analysis of Fcγ receptor and T cell receptor interacting with respective ligands." Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/26716.

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Low affinity Fcg receptor III (FcgRIII, CD16) triggers a variety of cellular events upon binding to the Fc portion of IgG. A real-time flow cytometry method was developed to measure the affinity and kinetics of such low affinity receptor/ligand interactions, which was shown as an easily operated yet powerful tool. Results revealed an unusual temperature dependence of reverse rate of CD16aTM dissociating from IgG. Except for a few studies using mammalian cell CD16s, most kinetics analyses use purified aglycosylated extracellular portion of the molecules, making it impossible to assess the importance of the receptor anchor and glycosylation on ligand binding. We used a micropipette adhesion frequency assay to demonstrate that the anchor length affects the forward rate and affinity of CD16s for IgG in a species specific manner, most likely through conformational changes. Receptor glycosylation dramatically reduced ligand binding by 100 folds. T cell receptor (TCR) is arguably the most important receptor in the adaptive human immune system. Together with coreceptor CD4 or CD8, TCR can discriminate different antigen peptides complexed with major histocompatibility complex (MHC) molecule (pMHC), which differ by as few as only one amino acid, and trigger different T cell responses. When T cell signaling was suppressed, TCR had similar affinity and kinetics for agonist and antagonist pMHC whose binding to CD8 was undetectable. TCR on activated T cell had a higher affinity for pMHCs, suggesting that TCRs organize themselves differently on activated T cells than on naïve T cells. In the absence of inhibitors for signaling, TCR binds agonist pMHC with several orders of magnitude higher affinity than antagonist pMHC. In addition, engagement of TCR by pMHC signals an upregulation of CD8 binding to pMHC, which is much stronger than the TCR-pMHC binding. The transition from weak TCR binding to the strong CD8 binding takes place around 0.75 second after TCR in contact with pMHC and can be reduced by several inhibitors of tyrosine and lipid phosphorylation, membrane rafts, and actin cytoskeleton. These results provide new insights to understanding T cell discrimination.
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Weaver, Richard Emyr. "Ligand-receptor interactions at the parathyroid hormone receptors." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531595.

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Björnström, Linda. "Molecular mechanisms of alternative estrogen receptor signaling /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-509-3/.

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Chu, Kwun Pok. "Computational studies of nuclear receptors : estrogen receptors, glucocorticoid receptors, and farnesoid X receptor." HKBU Institutional Repository, 2009. http://repository.hkbu.edu.hk/etd_ra/1058.

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Books on the topic "NO receptor"

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Fuxe, Kjell, and Luigi F. Agnati, eds. Receptor-Receptor Interactions. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9.

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Fuxe, Kjell, and Luigi F. Agnati, eds. Receptor-Receptor Interactions. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5415-4.

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Renato, Lauro, and Pirro Roberto De, eds. Handbook on receptor research: Insulin receptors. Roma: Field Educational Italia, Acta Medica, 1985.

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1928-, Thompson James C., and Galveston International Symposium on Gastrointestinal Endocrinology: Receptors and Post-Receptor Mechanisms (2nd : 1989), eds. Gastrointestinal endocrinology: Receptors and post-receptor mechanisms. San Diego: Academic Press, 1990.

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Conn, P. Michael. Receptor Molecular Biology: Receptor Molecular Biology. Burlington: Elsevier, 1995.

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Martin, Sarter, Nutt David J. 1951-, and Lister Richard G, eds. Benzodiazepine receptor inverse agonists. New York: Wiley-Liss, 1995.

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Boulton, Alan A., Glen B. Baker, and Pavel D. Hrdina. Receptor Binding. New Jersey: Humana Press, 1986. http://dx.doi.org/10.1385/0896030784.

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Litwack, Gerald, ed. Receptor Purification. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-0461-9.

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Litwack, Gerald, ed. Receptor Purification. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-0477-0.

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Colombo, Giancarlo, ed. GABAB Receptor. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46044-4.

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Book chapters on the topic "NO receptor"

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Müller, Judith M., and Roland Schüle. "Sex Steroid Receptors: Androgen Receptor, Estrogen Receptors, Progesterone Receptor." In Encyclopedia of Molecular Pharmacology, 1415–21. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_163.

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Müller, Judith M., and Roland Schüle. "Sex Steroid Receptors: Androgen Receptor, Estrogen Receptors, Progesterone Receptor." In Encyclopedia of Molecular Pharmacology, 1–7. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-21573-6_163-1.

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Hollenberg, M. D. "Receptor Regulation and Receptor-Receptor Communication." In Receptor-Receptor Interactions, 546–54. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9_43.

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Hollenberg, M. D. "Receptor Regulation and Receptor-Receptor Communication." In Receptor-Receptor Interactions, 546–54. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5415-4_43.

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Bloom, Floyd E., John Morrison, Elena Battenberg, David Lewis, and Michael Campbell. "Interactions between Convergent Afferent Transmitter Systems." In Receptor-Receptor Interactions, 3–12. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9_1.

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Moss, Robert L., Carol A. Dudley, Yang-In Kim, and Misty Eaton. "Estrogenic and Antiestrogenic Modulation of Neuronal Membrane Sensitivity." In Receptor-Receptor Interactions, 105–18. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9_10.

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Vincent, J. D., J. Demotes-Mainard, E. Arnauld, and J. M. Israel. "Effects of Estrogens on the Electrophysiological Properties of Neurons and Adenohypophyseal Cells: Interactions with Dopamine." In Receptor-Receptor Interactions, 119–30. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9_11.

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Cooney, Deirdre, Andreas Holzhöfer, Fritz Boege, Christian Dees, Rolf Jürss, Alan K. Keenan, Mirko Hekman, and Ernst J. M. Helmreich. "Receptor Modification and Receptor Disposition in Membranes." In Receptor-Receptor Interactions, 133–44. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9_12.

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Berridge, M. J. "Membrane Phospholipid Metabolism and Transmitters." In Receptor-Receptor Interactions, 145–61. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9_13.

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Changeux, J. P., J. Giraudat, M. Dennis, M. Goeldner, C. Hirth, C. Mulle, F. Révah, A. Devillers-Thiéry, and T. Heidmann. "Allosteric Sites and Conformational Transitions of the Acetylcholine Receptor: Models for Short-term Regulation of Receptor Response." In Receptor-Receptor Interactions, 162–90. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9_14.

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Conference papers on the topic "NO receptor"

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Basu, Gargi D., Ariane Kemkes, Rebecca A. Feldman, David R. Arguello, Alan Wright, David Loesch, and Raheela Ashfaq. "Abstract 3152: Distribution of hormone receptors (estrogen receptor, progesterone receptor and androgen receptor) in epithelial malignancies." 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.am2011-3152.

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Chesla, Scott E., Bryan T. Marshall, and Cheng Zhu. "Measuring the Probability of Receptor Extraction From the Cell Membrane." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0262.

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Abstract Recently, there has been an increasing interest in measuring the interaction forces between cell adhesion receptors and their ligands [1–3]. These molecules are either anchored on the membrane of a cell or coated on the surface of a substratum. The two surfaces are joined together as a result of the formation of non-covalent bonds between the receptors and ligands. The forces are measured when the two surfaces are separated. In a theoretical paper published nineteen years ago, George Bell estimated the force required to break a receptor-ligand bond and that required to uproot the receptor from the cell membrane to be of the same order of magnitude [4]. The interpretation of the force data therefore requires the knowledge of detachment mode, i.e., via adhesive mechanism if the receptor-ligand bond is dissociated or via cohesive mechanism if the receptor-membrane anchor is disrupted.
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Brill, Michael H., Doreen W. Bergeron, and William W. Stoner. "Trichromatic retinal model with adaptive contrast sensitivity and resolution." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/oam.1987.thc4.

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A computer-simulated retina called IRIS is described which discriminates small differences in reflected light when these differences occur in a restricted domain of space and time and maintains sensitivity to these differences for a wide range of light environments. As prevailing light levels de crease and photon noise becomes significant, IRIS automatically reduces its spatiotemporal resolution to provide greater redundancy. The temporal resolution depends on light intensity because each receptor’s response is governed by photopigment kinetics whose rate increases with light level. The spatial resolution depends on light intensity because the receptors are individual circuits (with voltage sources and photoconductors) coupled by a passive conducting grid. At high light intensity, the conductances within each receptor circuit are much greater than the lateral conductance, hence the receptor circuits are effectively uncoupled. Decreasing light intensity causes the lateral conductance to become more significant, thereby coupling the receptors and reducing spatial resolution. The simulation (implemented in FORTRAN) is adapted from the dissertation work of one of the authors.1 Simulation results are presented, and parallels to human vision are noted—including implications for trichromatic vision. The conducting grid might be achieved by tight-junction coupling of receptors and horizontal-cell interconnections that form an effective syncytium.
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Srinivasan, Visvanathan, Nayan Reddy, Adriana Brasoava, and David L. Wells. "Micro-Embossing of Polymeric Substrates for Fluidic Self-Assembly." In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-14817.

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Fluidic Self-Assembly™ (FSA)™ has become a routine manufacturing process in the production of radio-frequency identification tags. FSA operates through the self-positioning of micro-devices into pre-prepared matching receptor sites in a substrate. Research at North Dakota State University has focused on extending the applications of FSA well-beyond the current production routine. This pursuit requires, among other modifications, substantive extrapolation of the size, depth, configuration, spacing and spatial density of receptor sites. Three different test wafer patterns (see Figure 5 for patterns having nominal sizes of 1050μ, 1500μ, μ2150 and 3050μ square receptors with different spacing between them) took into account the corner compensation structure dimensions, which are based on thickness of silicon mold wafer feature to be etched (see Figure 2). The embossing tool (silicon wafer) was patterned photo-lithographically and subsequently wet etched in a KOH 2:1 solution. Experiments suggest shorter tool life in the case of closely packed features (spacing ~ 0.5mm). Receptor profiles evaluated using both optical and mechanical inspection (see Figures 3 and 4) suggest that features having larger size (up to nominal size of 3050μ square) and thickness (nominal depths of 110μ and 210μ) can be embossed accurately for use in FSA by slightly increasing the embossing time in case of deeper receptors. It was also noticed that the relative receptor depths attained with respect to the thickness of the feature on the mold wafer was lower while embossing deeper receptor sites, leading to the conclusion that mold wafers must be etched longer in such cases. The embossed receptor sites were subsequently filled with micro-devices in accordance with the standard operating parameters of Fluidic Self-Assembly process. These sample experimental runs suggest receptors slightly deeper than the micro-devices facilitate higher yields (or fill rates) in FSA. However, in cases where the receptors are too deep relative to the micro-device (> 5μ), air-entrapment occurred between the micro-device and the bottom of the receptor site, which caused problems in post-FSA processes due to air expansion. This paper presents comprehensive guidelines for embossing larger and deeper receptors for effective use in FSA.
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Watson, Andrew B. "Constraints on sensitivity of linear visual neurons." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/oam.1988.tuh4.

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Many visual neurons linearly combine signals from the receptors or from other cells which themselves form linear combinations of receptor signals. In both cases, if the noise that limits cell performance is confined to the receptors, the peak sensitivity of the cell is entirely determined by the magnitude of the receptor noise and the normalized shape of the cells’ receptive field. This simple result may be used to estimate the receptor noise from the sensitivity of retinal or geniculate cells as well as to predict sensitivity of higher-order cells from that of lower-order cells. Consequences of this constraint are illustrated for actual primate geniculate and cortical cells and for model cortical cells.
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Hawiger, J. "PLATELET RECEPTOR RECOGNITION DOMAINS AND THEIR SYNTHETIC PEPTIDE ANALOGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643726.

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Adhesive molecules and their receptorsplay an essential role in hemostasis and thrombosis. Platelet thrombi are formed through the interaction of cell adhesion molecules (CAMs) with intercellular adhesion molecules (IAMs)and substrate adhesion molecules (SAMs). Platelet CAMs encompass membrane glycoproteins lb, lib, Ilia,and possibly la and IV, which constitutemembrane receptors for IAMs(e.g., fibrinogen) and for SAMs encompassingvon Willebrand Factor (vWF), fibronectin, vitronectin, collagen, and thrcmbospondin. Receptorfunction of platelet CAMs can be specific,i.e., only one adhesive protein among IAMs and SAMs is selected forbinding as exemplified by GPIb and vWF. Alternatively,more than one adhesive protein can interact with platelet CAMs comprising the GPIIb/IIIa complex.This common adhesive receptor mechanism switched on by thrombin, ADP, phorbol ester or ionophore A23187 is turned off by a rise in intraplatelet cyclic AMP which provides a negative control.Fibrinogen, the most abundant adhesiveprotein in plasma, interacts with platelet CAMs via receptor recognition domains on gamma and alpha chains. Pinpointing platelet receptor recognition domain to a carboxy-terminal segment of the gamma chain encompassing residues 400-411gave rise to a series of synthetic peptide analogs which do not interfere with themetabolic pathways of platelets but blockbinding of I fibrinogen to its receptors on stimulated platelets, inhibit their aggregation in vitro, and formation of a platelet thrombus in vivo. The alpha chain of human fibrinogen contains the sequenceRGD (residues 95-97 and 572-574). Synthetpeptide analogs of the RGD sequence, which constitute the "cell adhesion site" of fibronectin, also inhibit binding of 125I-fibrinogen to stimulated platelets. However, these synthetic peptides are not "specific" for fibrinogen chains because thealpha chain of human fibrinogen which hasnosequence homology with gamma 400-411 is prevented by a peptide gamma 400-411 from interaction with platelet receptors. Viceversa, the human gamma chain is blocked by tetrapeptide RGDS not expressed in the human gamma chain. Interaction of human vWF with human platelets is blocked by synthetic peptide analogs of gamma 400-411 (not present in vWF)and of RGD sequence (present in vWF).These synthetic peptides inhibite "common" receptor pathwaystimulated with ADP, thrombin, or phorbolester, but they do not interfere with binding of 125I-vWF via a "specific" pathvoy induced with ristocetin and involving GPIb.The design of synthetic peptide analogs which inhibit platelet receptors for adhesive molecules includes the following considerations: ligand specificity (is thepeptide inhibitory toward binding of one or more adhesive molecules?),cell speciicity (is the peptide specific for platelets or does it perturb the adhesive properties of other cells, e.g.,endothelium?);the hydrophilic character; protection against degradation by peptidases; and a sufficiently long half-life to achieve platelet inhibitory potency in vivo without overloading the blood with excessive amounts of peptide.This is accomplished by constructing a peptide-albumin conjugate with ahalf-life extended at least 30 times.Whenpeptides are modeled with predominantly hydrophilic or hydrophobic residues, only the hydrophilic peptide remained active to block the platelet receptor. This agreed with the general observation that sequences on adhesive molecules that are knownto interact with cellular receptors have a hydrophilic rather than a hydrophobic character. Furthermore, changing the charge of synthetic peptides toward the negative reduced the reactivity, whereas introducing additional arginine residues enhanced the reactivity toward platelet receptors. Localization of the functionally important binding domain in the flexible segment of an adhesive protein increases the likelihood that the synthetic peptide will assume the conformation mimicking such a domain in the native adhesive protein. Structure-function studies of the receptor recognition domains on adhesive molecules led to development of a new class of platelet inhibitors acting at the membranereceptors responsible for anchoring of platelets to the vessel wall and linking them to each other.
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Hood, Donald C., and David G. Birch. "The a-wave of the ERG as a quantitative measure of human receptor activity." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/navs.1990.mc4.

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For over fifty years, the leading edge of the a-wave has been associated with receptor activity1. Uncertainty remains, however, about the answers to two basic questions: First, to what extent does the a-wave reflect receptor activity? For example, can we assume that the amplitude of the a-wave is linearly related to the size of the receptor's response? And, second, can we associate specific defects in receptor function with alterations in the leading edge of the a-wave? We are addressing these questions by comparing the leading edge of the rod a-wave to models of the rod receptor2,3.
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Hood, Donald C., and David G. Birch. "Adaptation of human cone receptors: Recordings of cone a-waves." In Advances in Color Vision. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/acv.1992.fa4.

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Boynton and Whitten1 were the first to attempt a quantitative description of the physiology of of primate cone adaptation. Using Brown's technique2 to isolate the summed receptor potential responsible for the cone a-wave of the monkey's ERG, they concluded that substantial adaptation occurred at the level of the cone receptor. The amount of adaptation and the mechanisms involved, however, are still open to debate. Here we focus on the mechanisms of adaptation of human cone receptors.
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Stine, Wm Wren, and John E. Sparrow. "Influence Theory for Retinex Models." In Color Appearance. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/ca.1987.tua3.

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The color constancy problem is one of calculating reflectance values for surfaces under differing illuminants. Retinex theory (e.g., Land, 1986) states that relative receptor responses are used to recover surface reflectance after they have been normalized with respect to the responses of neighboring receptor responses. Specifically, a number of paths to the pixel in question are randomly chosen and the logarithm of the ratio of the pixel receptor's response to the geometric mean of the receptor responses over a large number of paths is used as the lightness value for the pixel in question. Symbolically (1) where r(x,k) is the response of receptor x (to pixel x) of class k (where k is either the short wavelength, medium wavelength, or long wavelength cone), G(p,k) is the geometric mean of all of the receptor responses of class k covered by the random paths p, and l(x,k) is the resulting lightness value for receptor x (to pixel x) of class k. By normalizing the lightness value to the geometric mean of the neighboring receptor responses the change of the lightness value in response to overall spectral changes in illumination is minimized.
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De Chaffoy de Courcells, D., and F. De Clerck. "THE EFFECT OF A COMBINED TXA2SYNTHETASE AND TXA2/PROSTAGLANDIN ENDOPEROXIDE RECEPTOR BLOCKER(R 68 070)ON THE ACTIVATION OF EXCITATORY RECEPTOR-COUPLEDPHOSPHOLIPASE C IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643758.

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Prostaglandin endoperoxides (PGEND) and thromboxane A2 (TxA2)contribute to the activation of platelets, involving inositol-containing phospholipids as a signal transducing system. A primary step in this signal transduction consists of the activation of phospholipase C, which then yields diacylglycerol and inositol phosphates;diacylglycerol is subsequently phosphorylated to phosphatidic acid (PA). In platelets prelabelled with [32P] orthophosphate,receptor activation is quantitatively reflected by an increased formation of [32P]-PA.Using this assay, the relativeimportance of endogenously generated PGEND and TxA2 for the subsequent PA-formation was analysed by means of pharmacological manipulations. R 68 070, an oxime-alkanecarboxylic acid derivative combining specific TxA2 synthetase inhibition with TxA2/PGEND receptor blockade in one molecule (1 x 10-6M) inhibited the formation of PA in collagen-stimulated platelets; by contrast, synthetase inhibitors without receptor effect (da-zoxiben, OKY-1581,1x 10-6M) increased the PA-response tocollagen.Using U 46619 as a stimulus, R 68 070 as well as BM 13177, a receptor blocker withouteffect on synthetase (1 x 10-6 M)both reduced the PA-response to the same extent while OKY-1581 (1 x 10-6 M) was ineffective. The phospholipid response induced by serotonin, vasopressin or PAF were not affected by R 68 070, demonstrating its specificity for the prostanoid system.From these data we suggest that selectiveinhibition of TxA2 synthetase does not prevent activation of excitatory platelet receptors for arachidonate metabolites. Effectiveness was only obtained by combined TxA2 synthetase/PGEND receptor blockade.
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Reports on the topic "NO receptor"

1

Safe, Stephen H. Inhibitory Ah Receptor - Androgen Receptor Crosstalk in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada423669.

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Holaday, John W. Opiate Receptor Subtypes. Fort Belvoir, VA: Defense Technical Information Center, March 1985. http://dx.doi.org/10.21236/ada165206.

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Cohen, Saul G. Acetylcholinesterase and Acetylcholine Receptor. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada255623.

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Cohen, Saul G. Acetylcholinesterase and Acetylcholine Receptor. Fort Belvoir, VA: Defense Technical Information Center, January 1985. http://dx.doi.org/10.21236/adb112772.

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DiRenzo, James. Inhibition of Estrogen Receptor Action by the Orphan Receptors, SHP and DAX-1. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada403608.

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DiRenzo, James. Inhibition of Estrogen Receptor Action by the Orphan Receptors, SHP and DAX-1. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412765.

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DiRenzo, James. Inhibition of Estrogen Receptor Action by the Orphan Receptors, SHP and DAX-1. Fort Belvoir, VA: Defense Technical Information Center, December 2003. http://dx.doi.org/10.21236/ada419517.

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Direnzo, James. Inhibition of Estrogen Receptor Action by the Orphan Receptors, SHP and DAX-1. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada393316.

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Stearns, Carrie. Role of the Non-Receptor Tyrosine Kinase ACK2 in EGF Receptor Degradation. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada427754.

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Stearns, Carrie. Role of the Non-Receptor Tyrosine Kinase ACK2 in EGF Receptor Degradation. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada435047.

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