scholarly journals Divergence in Coding Sequence and Expression of Different Functional Categories of Immune Genes between Two Wild Rodent Species

2021 ◽  
Vol 13 (3) ◽  
Author(s):  
Xiuqin Zhong ◽  
Max Lundberg ◽  
Lars Råberg
Keyword(s):  
Signal Transduction ◽  
Transcription Factors ◽  
Immune Function ◽  
Sequence Divergence ◽  
Expression Divergence ◽  
Functional Categories ◽  
Coding Sequence ◽  
Immune Genes ◽  
Genes Encoding ◽  
Signal Transduction Proteins

Abstract Differences in immune function between species could be a result of interspecific divergence in coding sequence and/or expression of immune genes. Here, we investigate how the degree of divergence in coding sequence and expression differs between functional categories of immune genes, and if differences between categories occur independently of other factors (expression level, pleiotropy). To this end, we compared spleen transcriptomes of wild-caught yellow-necked mice and bank voles. Immune genes expressed in the spleen were divided into four categories depending on the function of the encoded protein: pattern recognition receptors (PRR); signal transduction proteins; transcription factors; and cyto- and chemokines and their receptors. Genes encoding PRR and cyto-/chemokines had higher sequence divergence than genes encoding signal transduction proteins and transcription factors, even when controlling for potentially confounding factors. Genes encoding PRR also had higher expression divergence than genes encoding signal transduction proteins and transcription factors. There was a positive correlation between expression divergence and coding sequence divergence, in particular for PRR genes. We propose that this is a result of that divergence in PRR coding sequence leads to divergence in PRR expression through positive feedback of PRR ligand binding on PRR expression. When controlling for sequence divergence, expression divergence of PRR genes did not differ from other categories. Taken together, the results indicate that coding sequence divergence of PRR genes is a major cause of differences in immune function between species.

scholarly journals The molecular mechanisms of multidrug resistance of human glioblastomas

2021 ◽  
Vol 67 (1) ◽  
pp. 20-28
Author(s):  
Alexandr Chernov ◽  
Irina Baldueva ◽  
Tatyana Nekhaeva ◽  
Elvira Galimova ◽  
Diana Alaverdian ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Drug Resistance ◽  
Transcription Factors ◽  
Growth Factors ◽  
Multidrug Resistance ◽  
Tumor Suppressor Genes ◽  
Molecular Mechanisms ◽  
Molecular Targets ◽  
Polymorphic Variants ◽  
Signal Transduction Proteins

In review discusses the phenomenon of drug resistance of GB in the context of the expression of ABC family transporter proteins and the processes of proliferation, angiogenesis, recurrence and death. The emphasis is on the identifying for molecular targets among growth factors, receptors, signal transduction proteins, microRNAs, transcription factors, proto-oncogenes, tumor suppressor genes and their polymorphic variants (SNPs) for the development and creation of targeted anticancer drugs.

scholarly journals Identification of Genes That Confer Sediment Fitness to Desulfovibrio desulfuricans G20

2007 ◽  
Vol 73 (19) ◽  
pp. 6305-6312 ◽  
Author(s):  
Qingwei Luo ◽  
Jennifer L. Groh ◽  
Jimmy D. Ballard ◽  
Lee R. Krumholz
Keyword(s):  
Signal Transduction ◽  
Dna Repair ◽  
Amino Acid ◽  
Desulfovibrio Desulfuricans ◽  
Amino Acid Biosynthesis ◽  
Hydrogenase Activity ◽  
Functional Categories ◽  
Acid Biosynthesis ◽  
Genes Encoding ◽  
Insertion Elements

ABSTRACT Signature-tagged mutants of Desulfovibrio desulfuricans G20 were screened, and 97 genes crucial for sediment fitness were identified. These genes belong to functional categories including signal transduction, binding and transport, insertion elements, and others. Mutants with mutations in genes encoding proteins involved in amino acid biosynthesis, hydrogenase activity, and DNA repair were further characterized.

scholarly journals PIM3 Proto-Oncogene Kinase Is a Common Transcriptional Target of Divergent EWS/ETS Oncoproteins

2003 ◽  
Vol 23 (11) ◽  
pp. 3897-3908 ◽  
Author(s):  
Benjamin Deneen ◽  
Scott M. Welford ◽  
Thu Ho ◽  
Felicia Hernandez ◽  
Irwin Kurland ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Target Genes ◽  
Lactate Production ◽  
Structural Diversity ◽  
Serine Threonine Kinase ◽  
Threonine Kinase ◽  
Genes Encoding ◽  
Signal Transduction Proteins ◽  
Nih 3T3 ◽  
Microarray Expression

ABSTRACT Despite significant structural diversity, present evidence suggests that EWS/ETS fusion proteins promote oncogenesis by transcriptionally modulating a common set of target genes. In order to identify these genes, microarray expression analyses were performed on NIH 3T3 polyclonal populations expressing one of three EWS/ETS fusion genes. The majority of these genes can be grouped into seven functional categories, including cellular metabolism and signal transduction. The biologic significance of these target genes was pursued. The effects of modulating genes involved in metabolism were assessed by flux studies and demonstrated shifts in glucose utilization and lactate production as a result of EWS/FLI1 expression. The proto-oncogene coding for serine/threonine kinase PIM3 was found to one of several genes encoding signal transduction proteins that were up-regulated by EWS/ETS fusions. PIM3 was found to be expressed in a panel of human Ewing's family tumor cell lines. Forced expression of PIM3 promoted anchorage-independent growth. Coexpression of a kinase-deficient PIM3 mutant attenuated EWS/FLI1-mediated NIH 3T3 tumorigenesis in immunodeficent mice.

Dietary zinc deficiency and expression of T lymphocyte signal transduction proteins

2000 ◽  
Vol 78 (10) ◽  
pp. 823-828 ◽  
Author(s):  
Carla G Taylor ◽  
Jeri-Anne C Giesbrecht
Keyword(s):  
Signal Transduction ◽  
T Lymphocytes ◽  
Immune Function ◽  
T Lymphocyte ◽  
Molecular Level ◽  
Immune Dysfunction ◽  
Zn Deficiency ◽  
Dietary Zinc ◽  
Signal Transduction Proteins

Impaired immune function in dietary zinc (Zn) deficiency is characterized in part by reduced lymphocyte numbers (lymphopenia) and depressed cell-mediated (T lymphocyte) immune function, however, the causative mechanisms at the molecular level have not been elucidated. This paper will focus on the role of dietary Zn in T lymphocyte signal transduction, and specifically, the early Zn-dependent steps for phosphorylation and the putative Zn-finger proteins or Zn-metalloenzymes that may be part of the molecular mechanism for explaining immune dysfunction in Zn deficiency. One of the major recent findings is that murine splenic T lymphocyte p56lck expression is elevated in dietary Zn deficiency and caloric deficiency. Based on the known functions of p56lck, it is proposed that elevated p56lck may contribute to altered thymocyte maturation, apoptosis, and lymphopenia in dietary Zn deficiency and other malnutrition syndromes.Key words: zinc, T lymphocytes, signal transduction, immune function.

scholarly journals Genes encoding components of the olfactory signal transduction cascade contain a DNA binding site that may direct neuronal expression.

1993 ◽  
Vol 13 (9) ◽  
pp. 5805-5813 ◽  
Author(s):  
M M Wang ◽  
R Y Tsai ◽  
K A Schrader ◽  
R R Reed
Keyword(s):  
Signal Transduction ◽  
Dna Binding ◽  
Binding Site ◽  
Binding Sites ◽  
Consensus Sequence ◽  
Initiation Site ◽  
Olfactory Neuron ◽  
Promoter Regions ◽  
Transcriptional Initiation ◽  
Genes Encoding

Genes which mediate odorant signal transduction are expressed at high levels in neurons of the olfactory epithelium. The molecular mechanism governing the restricted expression of these genes likely involves tissue-specific DNA binding proteins which coordinately activate transcription through sequence-specific interactions with olfactory promoter regions. We have identified binding sites for the olfactory neuron-specific transcription factor, Olf-1, in the sequences surrounding the transcriptional initiation site of five olfactory neuron-specific genes. The Olf-1 binding sites described define the consensus sequence YTCCCYRGGGAR. In addition, we have identified a second binding site, the U site, in the olfactory cyclic nucleotide gated channel and type III cyclase promoters, which binds factors present in all tissue examined. These experiments support a model in which expression of Olf-1 in the sensory neurons coordinately activates a set of olfactory neuron-specific genes. Furthermore, expression of a subset of these genes may be modulated by additional binding factors.

scholarly journals Role of Satb1 and Satb2 Transcription Factors in the Glutamate Receptors Expression and Ca2+ Signaling in the Cortical Neurons In Vitro

2021 ◽  
Vol 22 (11) ◽  
pp. 5968
Author(s):  
Egor A. Turovsky ◽  
Maria V. Turovskaya ◽  
Evgeniya I. Fedotova ◽  
Alexey A. Babaev ◽  
Viktor S. Tarabykin ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Nmda Receptor ◽  
Cortical Neurons ◽  
Target Genes ◽  
Cortical Cell ◽  
Inhibitory System ◽  
Selective Agonist ◽  
Genes Encoding ◽  
Deficient Mice

Transcription factors Satb1 and Satb2 are involved in the processes of cortex development and maturation of neurons. Alterations in the expression of their target genes can lead to neurodegenerative processes. Molecular and cellular mechanisms of regulation of neurotransmission by these transcription factors remain poorly understood. In this study, we have shown that transcription factors Satb1 and Satb2 participate in the regulation of genes encoding the NMDA-, AMPA-, and KA- receptor subunits and the inhibitory GABA(A) receptor. Deletion of gene for either Satb1 or Satb2 homologous factors induces the expression of genes encoding the NMDA receptor subunits, thereby leading to higher amplitudes of Ca2+-signals in neurons derived from the Satb1-deficient (Satb1fl/+ * NexCre/+) and Satb1-null mice (Satb1fl/fl * NexCre/+) in response to the selective agonist reducing the EC50 for the NMDA receptor. Simultaneously, there is an increase in the expression of the Gria2 gene, encoding the AMPA receptor subunit, thus decreasing the Ca2+-signals of neurons in response to the treatment with a selective agonist (5-Fluorowillardiine (FW)). The Satb1 deletion increases the sensitivity of the KA receptor to the agonist (domoic acid), in the cortical neurons of the Satb1-deficient mice but decreases it in the Satb1-null mice. At the same time, the Satb2 deletion decreases Ca2+-signals and the sensitivity of the KA receptor to the agonist in neurons from the Satb1-null and the Satb1-deficient mice. The Satb1 deletion affects the development of the inhibitory system of neurotransmission resulting in the suppression of the neuron maturation process and switching the GABAergic responses from excitatory to inhibitory, while the Satb2 deletion has a similar effect only in the Satb1-null mice. We show that the Satb1 and Satb2 transcription factors are involved in the regulation of the transmission of excitatory signals and inhibition of the neuronal network in the cortical cell culture.

scholarly journals MECHANISMS IN ENDOCRINOLOGY: An update in the genetic aetiologies of combined pituitary hormone deficiency

2016 ◽  
Vol 174 (6) ◽  
pp. R239-R247 ◽  
Author(s):  
Frederic Castinetti ◽  
Rachel Reynaud ◽  
Alexandru Saveanu ◽  
Nicolas Jullien ◽  
Marie Helene Quentien ◽  
...  
Keyword(s):  
Transcription Factors ◽  
G Protein Coupled Receptors ◽  
Hormone Deficiency ◽  
Immunoglobulin Superfamily ◽  
Pituitary Hormone ◽  
Pituitary Hormone Deficiency ◽  
Combined Pituitary Hormone Deficiency ◽  
Signalling Molecules ◽  
Genes Encoding ◽  
G Protein Coupled

Over the last 5 years, new actors involved in the pathogenesis of combined pituitary hormone deficiency in humans have been reported: they included a member of the immunoglobulin superfamily glycoprotein and ciliary G protein-coupled receptors, as well as new transcription factors and signalling molecules. New modes of inheritance for alterations of genes encoding transcription factors have also been described. Finally, actors known to be involved in a very specific phenotype (hypogonadotroph hypogonadism for instance) have been identified in a wider range of phenotypes. These data thus suggest that new mechanisms could explain the low rate of aetiological identification in this heterogeneous group of diseases. Taking into account the fact that several reviews have been published in recent years on classical aetiologies of CPHD such as mutations ofPOU1F1orPROP1, we focused the present overview on the data published in the last 5 years, to provide the reader with an updated review on this rapidly evolving field of knowledge.

scholarly journals Genes Encoding Transcription Factors TaDREB5 and TaNFYC-A7 Are Differentially Expressed in Leaves of Bread Wheat in Response to Drought, Dehydration and ABA

2018 ◽  
Vol 9 ◽  
Author(s):  
Lyudmila Zotova ◽  
Akhylbek Kurishbayev ◽  
Satyvaldy Jatayev ◽  
Gulmira Khassanova ◽  
Askar Zhubatkanov ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Bread Wheat ◽  
Differentially Expressed ◽  
Genes Encoding

scholarly journals Characterization and risk association of polymorphisms in Aurora kinases A, B and C with genetic susceptibility to gastric cancer development

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Aner Mesic ◽  
Marija Rogar ◽  
Petra Hudler ◽  
Nurija Bilalovic ◽  
Izet Eminovic ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Transcription Factors ◽  
In Silico ◽  
In Silico Analysis ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Mitotic Kinases ◽  
Genes Encoding ◽  
Silico Analysis ◽  
Control Study

Abstract Background Single nucleotide polymorphisms (SNPs) in genes encoding mitotic kinases could influence development and progression of gastric cancer (GC). Methods Case-control study of nine SNPs in mitotic genes was conducted using qPCR. The study included 116 GC patients and 203 controls. In silico analysis was performed to evaluate the effects of polymorphisms on transcription factors binding sites. Results The AURKA rs1047972 genotypes (CT vs. CC: OR, 1.96; 95% CI, 1.05–3.65; p = 0.033; CC + TT vs. CT: OR, 1.94; 95% CI, 1.04–3.60; p = 0.036) and rs911160 (CC vs. GG: OR, 5.56; 95% CI, 1.24–24.81; p = 0.025; GG + CG vs. CC: OR, 5.26; 95% CI, 1.19–23.22; p = 0.028), were associated with increased GC risk, whereas certain rs8173 genotypes (CG vs. CC: OR, 0.60; 95% CI, 0.36–0.99; p = 0.049; GG vs. CC: OR, 0.38; 95% CI, 0.18–0.79; p = 0.010; CC + CG vs. GG: OR, 0.49; 95% CI, 0.25–0.98; p = 0.043) were protective. Association with increased GC risk was demonstrated for AURKB rs2241909 (GG + AG vs. AA: OR, 1.61; 95% CI, 1.01–2.56; p = 0.041) and rs2289590 (AC vs. AA: OR, 2.41; 95% CI, 1.47–3.98; p = 0.001; CC vs. AA: OR, 6.77; 95% CI, 2.24–20.47; p = 0.001; AA+AC vs. CC: OR, 4.23; 95% CI, 1.44–12.40; p = 0.009). Furthermore, AURKC rs11084490 (GG + CG vs. CC: OR, 1.71; 95% CI, 1.04–2.81; p = 0.033) was associated with increased GC risk. A combined analysis of five SNPs, associated with an increased GC risk, detected polymorphism profiles where all the combinations contribute to the higher GC risk, with an OR increased 1.51-fold for the rs1047972(CT)/rs11084490(CG + GG) to 2.29-fold for the rs1047972(CT)/rs911160(CC) combinations. In silico analysis for rs911160 and rs2289590 demonstrated that different transcription factors preferentially bind to polymorphic sites, indicating that AURKA and AURKB could be regulated differently depending on the presence of particular allele. Conclusions Our results revealed that AURKA (rs1047972 and rs911160), AURKB (rs2241909 and rs2289590) and AURKC (rs11084490) are associated with a higher risk of GC susceptibility. Our findings also showed that the combined effect of these SNPs may influence GC risk, thus indicating the significance of assessing multiple polymorphisms, jointly. The study was conducted on a less numerous but ethnically homogeneous Bosnian population, therefore further investigations in larger and multiethnic groups and the assessment of functional impact of the results are needed to strengthen the findings.

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