scholarly journals Cytokinin-Regulated Expression of Arabidopsis thaliana PAP Genes and Its Implication for the Expression of Chloroplast-Encoded Genes

Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1658
Author(s):  
Aleksandra A. Andreeva ◽  
Radomira Vankova ◽  
Ivan A. Bychkov ◽  
Natalia V. Kudryakova ◽  
Maria N. Danilova ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Nuclear Genes ◽  
Promoter Regions ◽  
Knock Out ◽  
Regulatory Circuit ◽  
Associated Proteins ◽  
Gene Transcripts ◽  
Plastid Rna Polymerase ◽  
Underlying Mechanisms

Cytokinins (CKs) are known to regulate the biogenesis of chloroplasts under changing environmental conditions and at different stages of plant ontogenesis. However, the underlying mechanisms are still poorly understood. Apparently, the mechanisms can be duplicated in several ways, including the influence of nuclear genes that determine the expression of plastome through the two-component CK regulatory circuit. In this study, we evaluated the role of cytokinins and CK signaling pathway on the expression of nuclear genes for plastid RNA polymerase-associated proteins (PAPs). Cytokinin induced the expression of all twelve Arabidopsis thalianaPAP genes irrespective of their functions via canonical CK signaling pathway but this regulation might be indirect taking into consideration their different functions and versatile structure of promoter regions. The disruption of PAP genes contributed to the abolishment of positive CK effect on the accumulation of the chloroplast gene transcripts and transcripts of the nuclear genes for plastid transcription machinery as can be judged from the analysis of pap1 and pap6 mutants. However, the CK regulatory circuit in the mutants remained practically unperturbed. Knock-out of PAP genes resulted in cytokinin overproduction as a consequence of the strong up-regulation of the genes for CK synthesis.

scholarly journals Conserved units of co-expression in bacterial genomes: an evolutionary insight into gene regulation

2014 ◽  
Author(s):  
Ivan Junier ◽  
Olivier Rivoire
Keyword(s):  
Gene Regulation ◽  
Strongly Correlated ◽  
Rna Seq ◽  
Regulatory Factor ◽  
Bacterial Genomes ◽  
Promoter Regions ◽  
Dna And Rna ◽  
Genome Wide ◽  
Associated Proteins ◽  
Underlying Mechanisms

Genome-wide measurements of transcriptional activity in bacteria indicate that the transcription of successive genes is strongly correlated beyond the scale of operons. However, the underlying mechanisms are poorly characterized and a systematic method for identifying local groups of co-transcribed genes is lacking. Here, we identify supra-operonic segments of consecutive genes by comparing gene proximity in thousands of bacterial genomes. Structurally, the segments are contained within micro-domains delineated by known nucleoid-associated proteins, and they contain operons with specific relative orientations. Functionally, the operons within a same segment are highly co-transcribed, even in the absence of regulatory factors at their promoter regions. Hence, operons with no common regulatory factor can be co-regulated if they share a regulatory factor at the level of segments. To rationalize these findings, we put forward the hypothesis supported by RNA-seq data that facilitated co-transcription, the feedback of transcription into itself involving only DNA and RNA-polymerases, may represent both an evolutionary primitive and a functionally primary mode of gene regulation.

scholarly journals BRCC3 Promotes Tumorigenesis of Bladder Cancer by Activating the NF-κB Signaling Pathway Through Targeting TRAF2

2021 ◽  
Vol 9 ◽  
Author(s):  
Huangheng Tao ◽  
Yixiang Liao ◽  
Youji Yan ◽  
Zhiwen He ◽  
Jiajie Zhou ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Patients ◽  
Signaling Pathway ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Rna Seq ◽  
Knock Out

NF-κB signaling is very important in cancers. However, the role of BRCC3-associated NF-κB signaling activation in bladder cancer remains to be characterized. Western blotting and IHC of tissue microarray were used to confirm the abnormal expression of BRCC3 in bladder cancer. Growth curve, colony formation, soft agar assay and Xenograft model were performed to identify the role of BRCC3 over-expression or knock-out in bladder cancer. Further, RNA-Seq and luciferase reporter assays were used to identify the down-stream signaling pathway. Finally, co-immunoprecipitation and fluorescence confocal assay were performed to verify the precise target of BRCC3. Here, we found that high expression of BRCC3 promoted tumorigenesis through targeting the TRAF2 protein. BRCC3 expression is up-regulated in bladder cancer patients which indicates a negative prognosis. By in vitro and in vivo assays, we found genetic BRCC3 ablation markedly blocks proliferation, viability and migration of bladder cancer cells. Mechanistically, RNA-Seq analysis shows that NF-κB signaling is down-regulated in BRCC3-deficient cells. BRCC3 binds to and synergizes with TRAF2 to activate NF-κB signaling. Our results indicate that high BRCC3 expression activates NF-κB signaling by targeting TRAF2 for activation, which in turn facilitates tumorigenesis in bladder cancer. This finding points to BRCC3 as a potential target in bladder cancer patients.

scholarly journals Pterostilbene Alleviates Cholestasis by Promoting SIRT1 Activity in Hepatocytes and Macrophages

2021 ◽  
Vol 12 ◽  
Author(s):  
Chuanrui Ma ◽  
Jiaqing Xiang ◽  
Guixiao Huang ◽  
Yaxi Zhao ◽  
Xinyu Wang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Cholestatic Liver Disease ◽  
P53 Signaling ◽  
Promising Target ◽  
Underlying Mechanisms ◽  
Cholestatic Liver Injury ◽  
P53 Signaling Pathway

Background and purpose: FXR is a promising target for the treatment of human cholestatic liver disease (CLD). SIRT1 is a deacetylase which promotes FXR activity through deacetylating FXR. Pterostilbene (PTE) is an activator of SIRT1. However, the role of PTE in cholestasis has so far not been investigated. We examined whether PTE treatment alleviate liver injury in DDC or ANIT-induced experimental cholestasis, and explored the underlying mechanisms.Experimental approach: Mice with DDC- or ANIT-induced cholestasis were treated with different dose of PTE. Primary hepatocytes and bone marrow derived macrophages were used in vitro to assess the molecular mechanism by which PTE may improve CLD. Identical doses of UDCA or PTE were administered to DDC- or ANIT-induced cholestasis mice.Key results: PTE intervention attenuated DDC or ANIT-induced cholestasis. PTE inhibited macrophage infiltration and activation in mouse liver through the SIRT1-p53 signaling pathway, and it improved hepatic bile metabolism through the SIRT1-FXR signaling pathway. Compare with UDCA, the same doses of PTE was more effective in improving cholestatic liver injury caused by DDC or ANIT.Conclusion and implications: SIRT1 activation in macrophages may be an effective CLD treatment avenue. Using CLD models, we thus identified PTE as a novel clinical candidate compound for the treatment of CLD.

scholarly journals P2X7R promotes angiogenesis and tumor-associated macrophage recruitment by regulating the NF-κB signaling pathway in colorectal cancer cells

2020 ◽  
Author(s):  
Chunhui Yang ◽  
shuang shi ◽  
Ying Su ◽  
jingshan tong ◽  
Liangjun Li
Keyword(s):  
Colorectal Cancer ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Orthotopic Model ◽  
Tumor Associated Macrophage ◽  
Underlying Mechanisms ◽  
Sphere Formation

Abstract Background Overexpression of P2 × 7R has been observed in several tumors and is related to cancer advancement and metastasis. However, the role of P2 × 7R in colorectal cancer (CRC) patients is not well understood. Methods In the current study, overexpression of P2 × 7R and the effects at the molecular and functional levels in CRC were assessed in a mouse orthotopic model. Functional assays, such as the CCK-8 assay, wound healing and transwell assay, were used to determine the biological role of P2 × 7R in CRC cells. CSC-related genes and properties were detected via sphere formation and real-time PCR assays. The underlying mechanisms were explored by Western blotting, real-time PCR and Flow cytometry. Results In this study, we found that overexpression of P2 × 7R increase in the in vivo growth of tumors. P2 × 7R overexpression also increased CD31, VEGF and concurrent angiogenesis. P2 × 7R upregulates aldehyde dehydrogenase-1 (ALDH1) and CSC characteristics. Transplanted tumor cells with P2 × 7R overexpression stimulated cytokines to recruit TAMs to increase the growth of tumors. We also found that the NF-κB signaling pathway is involved in P2 × 7R-induced cytokine upregulation. Conclusion P2 × 7R promotes NF-κB-dependent cytokine induction, which leads to tumor-associated macrophage (TAM) recruitment to control tumor growth and advancement and remodeling of the stroma. Our findings demonstrate that P2 × 7R plays a key role in TAM recruitment, which may be a therapeutic target for CRC patients.

scholarly journals Preventive Electroacupuncture Ameliorates D-Galactose-Induced Alzheimer’s Disease-Like Pathology and Memory Deficits Probably via Inhibition of GSK3β/mTOR Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Chao-Chao Yu ◽  
Jia Wang ◽  
Si-Si Ye ◽  
Shan Gao ◽  
Jia Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Dendritic Spines ◽  
Memory Deficits ◽  
Biological Action ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Phosphorylation Level ◽  
Associated Proteins ◽  
Autophagy Activity

Acupuncture has been practiced to treat neuropsychiatric disorders for a thousand years in China. Prevention of disease by acupuncture and moxibustion treatment, guided by the theory of Chinese acupuncture, gradually draws growing attention nowadays and has been investigated in the role of the prevention and treatment of mental disorders such as AD. Despite its well-documented efficacy, its biological action remains greatly invalidated. Here, we sought to observe whether preventive electroacupuncture during the aging process could alleviate learning and memory deficits in D-galactose-induced aged rats. We found that preventive electroacupuncture at GV20-BL23 acupoints during aging attenuated the hippocampal loss of dendritic spines, ameliorated neuronal microtubule injuries, and increased the expressions of postsynaptic PSD95 and presynaptic SYN, two important synapse-associated proteins involved in synaptic plasticity. Furthermore, we observed an inhibition of GSK3β/mTOR pathway activity accompanied by a decrease in tau phosphorylation level and prompted autophagy activity induced by preventive electroacupuncture. Our results suggested that preventive electroacupuncture can prevent and alleviate memory deficits and ameliorate synapse and neuronal microtubule damage in aging rats, which was probably via the inhibition of GSK3β/mTOR signaling pathway. It may provide new insights for the identification of prevention strategies of AD.

Critical role of high-mobility-group proteins in kidney development/cross-talk Wnt/β-catenin signaling pathway

2021 ◽  
Vol 9 (1) ◽  
pp. 123-134
Author(s):  
Mary Ann S. Arndt ◽  
William D. Wheaton
Keyword(s):  
Signaling Pathway ◽  
Kidney Development ◽  
Critical Role ◽  
High Mobility ◽  
Kidney Injury ◽  
High Mobility Group ◽  
Loss Of Function ◽  
Hmg Proteins ◽  
Associated Proteins

The treatment of severe acute kidney injury with dialytic support for renal replacement therapy can be life sustaining and permit recovery from critical illness. The high-mobility-group (HMG) proteins are the most abundant non-histone chromatin-associated proteins. HMG proteins are present at high levels in various undifferentiated tissues during embryonic development and reduced in the corresponding adult tissues. We used used in study C57BL/6, HMG+/− and HMG−/− mice and found that HMG is expressed in the mouse embryonic kidney at the cortex area. HMG knockout led to enhanced Wnt/β-catenin signaling pathway. Analysis of siRNA-mediated loss-of-function experiments in embryonic kidney culture confirmed the role of HMG as a key regulator of cortex epithelium differentiation.

Deciphering the role of aberrant protein post translational modification in the pathology of neurodegeneration

2020 ◽  
Vol 19 ◽  
Author(s):  
Sadat Shafi ◽  
Archu Singh ◽  
Paras Gupta ◽  
Pooja A. Chawla ◽  
Faizana Fayaz ◽  
...  
Keyword(s):  
Neurodegenerative Disorders ◽  
Posttranslational Modification ◽  
Protein Function ◽  
Post Translational Modification ◽  
Associated Proteins ◽  
Significant Step ◽  
Underlying Mechanisms ◽  
Lateral Sclerosis ◽  
Functional Alteration

: Neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD), are characterized by progressive neuronal dysfunction and death. Current studies have established detrimental modifications in brain protein function as well as structure which stimulate their aggregation, misfolding and deposition in and around the neurons, as an important hallmark of neurodegenerative disorders. Posttranslational modification (PTM) of proteins including phosphorylation, acetylation, glycosylation, palmitoylation, SUMOylation, and ubiquitination are important regulators of protein characteristics including stability, intracellular distribution, activity, interactions, aggregation and clearance. Despite clear evidence that altered protein modifications emerging from impromptu chemical modifications to side chains of amino acid is associated with neurodegeneration, the underlying mechanisms that promote aberrant PTM remain poorly understood. Therefore, elucidating PTM of specific disease associated proteins can prove to be a significant step in evaluating functional alteration of proteins and their association with neurodegeneration. This review describes how aberrant PTM of various proteins are linked with the neurodegenerative disease pathogenesis, as well as molecular strategies targeting these modifications for treating such diseases, which are yet incurable.

Critical role of high-mobility-group proteins in kidney development/cross-talk Wnt/β-catenin signaling pathway

2021 ◽  
Vol 9 (1) ◽  
pp. 135-144
Keyword(s):  
Signaling Pathway ◽  
Kidney Development ◽  
Critical Role ◽  
High Mobility ◽  
High Mobility Group ◽  
Loss Of Function ◽  
Hmg Proteins ◽  
Cortex Area ◽  
Associated Proteins

recovery from critical illness.The high-mobility-group (HMG) proteins are the most abundant non-histone chromatin-associated proteins. HMG proteins are present at high levels in various undifferentiated tissues during embryonic development and reduced in the corresponding adult tissues. We used used in study C57BL/6, HMG+/− and HMG−/−  mice and found that HMG is expressed in the mouse embryonic kidney at the cortex area. HMG knockout led to enhanced Wnt/β-catenin signaling pathway. Analysis of siRNA-mediated loss-of-function experiments in embryonic kidney culture confirmed the role of HMG as a key regulator of cortex epithelium differentiation.

285: The Role of the NF-κB Signaling Pathway in the Pathogenesis of Interstitial Cystitis

2006 ◽  
Vol 175 (4S) ◽  
pp. 95-95
Author(s):  
Raymond R. Rackley ◽  
Mei Kuang ◽  
Ashwin A. Vaze ◽  
Joseph Abdelmalak ◽  
Sandip P. Vasavada ◽  
...  
Keyword(s):  
Interstitial Cystitis ◽  
Signaling Pathway

Response Interference as a Mechanism Underlying Implicit Measures

2008 ◽  
Vol 24 (4) ◽  
pp. 218-225 ◽  
Author(s):  
Bertram Gawronski ◽  
Roland Deutsch ◽  
Etienne P. LeBel ◽  
Kurt R. Peters
Keyword(s):  
Task Performance ◽  
Psychological Research ◽  
Implicit Measures ◽  
Mediation Model ◽  
Response Interference ◽  
Relevant Evidence ◽  
Moderated Mediation Model ◽  
Stimulus Features ◽  
Underlying Mechanisms

Over the last decade, implicit measures of mental associations (e.g., Implicit Association Test, sequential priming) have become increasingly popular in many areas of psychological research. Even though successful applications provide preliminary support for the validity of these measures, their underlying mechanisms are still controversial. The present article addresses the role of a particular mechanism that is hypothesized to mediate the influence of activated associations on task performance in many implicit measures: response interference (RI). Based on a review of relevant evidence, we argue that RI effects in implicit measures depend on participants’ attention to association-relevant stimulus features, which in turn can influence the reliability and the construct validity of these measures. Drawing on a moderated-mediation model (MMM) of task performance in RI paradigms, we provide several suggestions on how to address these problems in research using implicit measures.

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