Insight into the biological pathways underlying fibromyalgia by a proteomic approach

2018 ◽  
Vol 186 ◽  
pp. 47-55 ◽  
Author(s):  
Jorge A. Ramírez-Tejero ◽  
Esther Martínez-Lara ◽  
Alma Rus ◽  
María Victoria Camacho ◽  
María Luisa Del Moral ◽  
...  
Keyword(s):  
Biological Pathways ◽  
Proteomic Approach ◽  
Insight Into

scholarly journals Multi-omics data integration reveals correlated regulatory features of triple negative breast cancer

2021 ◽  
Author(s):  
Kevin Chappell ◽  
Kanishka Manna ◽  
Charity L. Washam ◽  
Stefan Graw ◽  
Duah Alkam ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Data Integration ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Biological Pathways ◽  
Omics Data ◽  
Insight Into ◽  
Omics Data Integration

Multi-omics data integration of triple negative breast cancer (TNBC) provides insight into biological pathways.

scholarly journals SNX17 protects integrins from degradation by sorting between lysosomal and recycling pathways

2012 ◽  
Vol 197 (2) ◽  
pp. 219-230 ◽  
Author(s):  
Florian Steinberg ◽  
Kate J. Heesom ◽  
Mark D. Bass ◽  
Peter J. Cullen
Keyword(s):  
Isotope Labeling ◽  
Degradation Pathway ◽  
Lysosomal Degradation ◽  
Sorting Nexins ◽  
Retromer Complex ◽  
Proteomic Approach ◽  
Cytoplasmic Tails ◽  
Npxy Motif ◽  
Global Identification ◽  
Insight Into

The FERM-like domain–containing sorting nexins of the SNX17/SNX27/SNX31 family have been proposed to mediate retrieval of transmembrane proteins from the lysosomal pathway. In this paper, we describe a stable isotope labeling with amino acids in culture–based quantitative proteomic approach that allows an unbiased, global identification of transmembrane cargoes that are rescued from lysosomal degradation by SNX17. This screen revealed that several integrins required SNX17 for their stability, as depletion of SNX17 led to a loss of β1 and β5 integrins and associated a subunits from HeLa cells as a result of increased lysosomal degradation. SNX17 bound to the membrane distal NPXY motif in β integrin cytoplasmic tails, thereby preventing lysosomal degradation of β integrins and their associated a subunits. Furthermore, SNX17-dependent retrieval of integrins did not depend on the retromer complex. Consistent with an effect on integrin recycling, depletion of SNX17 also caused alterations in cell migration. Our data provide mechanistic insight into the retrieval of internalized integrins from the lysosomal degradation pathway, a prerequisite for subsequent recycling of these matrix receptors.

scholarly journals Molecular cloning of disintegrins from Cerastes vipera and Macrovipera lebetina transmediterranea venom gland cDNA libraries: insight into the evolution of the snake venom integrin-inhibition system

2006 ◽  
Vol 395 (2) ◽  
pp. 385-392 ◽  
Author(s):  
Libia Sanz ◽  
Amine Bazaa ◽  
Naziha Marrakchi ◽  
Alicia Pérez ◽  
Mehdi Chenik ◽  
...  
Keyword(s):  
Snake Venom ◽  
Binding Sites ◽  
Venom Gland ◽  
Cdna Libraries ◽  
Common Ancestry ◽  
Integrin Receptors ◽  
Proteomic Approach ◽  
Ligand Binding Sites ◽  
Insight Into ◽  
Laminin Binding

We report the cloning and sequence analysis of Cerastes vipera and Macrovipera lebetina transmediterranea cDNAs coding for short non-RGD (Arg-Gly-Asp) disintegrins and for dimeric disintegrin subunits. The mRNAs belong to the short-coding class, suggesting that these disintegrin mRNAs may be more widely distributed than previously thought. Our data also argue for a common ancestry of the mRNAs of short disintegrins and those coding for precursors of dimeric disintegrin chains. The Macrovipera lebetina transmediterranea dimeric disintegrin reported to inhibit the laminin-binding integrins α3β1, α6β1 and α7β1 was analysed using a proteomic approach and was shown to bear MLD (Met-Leu-Asp) and VGD (Val-Gly-Asp) motifs. The results highlight the fact that disintegrins have evolved a restricted panel of integrin-blocking sequences that segregate with defined branches of the phylogenetic tree of the integrin α-chains, providing novel insights into the evolutionary adaptation of the snake venom antagonists to the ligand-binding sites of their target integrin receptors.

scholarly journals Undulating changes in human plasma proteome across lifespan are linked to disease

2019 ◽  
Author(s):  
Benoit Lehallier ◽  
David Gate ◽  
Nicholas Schaum ◽  
Tibor Nanasi ◽  
Song Eun Lee ◽  
...  
Keyword(s):  
Human Plasma ◽  
Plasma Proteins ◽  
Biological Pathways ◽  
Phenotypic Traits ◽  
Plasma Proteome ◽  
New Approach ◽  
Disease Biology ◽  
Age Related ◽  
Insight Into ◽  
Human Plasma Proteome

Aging is the predominant risk factor for numerous chronic diseases that limit healthspan. Mechanisms of aging are thus increasingly recognized as therapeutic targets. Blood from young mice reverses aspects of aging and disease across multiple tissues, pointing to the intriguing possibility that age-related molecular changes in blood can provide novel insight into disease biology. We measured 2,925 plasma proteins from 4,331 young adults to nonagenarians and developed a novel bioinformatics approach which uncovered profound non-linear alterations in the human plasma proteome with age. Waves of changes in the proteome in the fourth, seventh, and eighth decades of life reflected distinct biological pathways, and revealed differential associations with the genome and proteome of age-related diseases and phenotypic traits. This new approach to the study of aging led to the identification of unexpected signatures and pathways of aging and disease and offers potential pathways for aging interventions.

scholarly journals Genetic Risk Profiling in Parkinson’s Disease and Utilizing Genetics to Gain Insight into Disease-Related Biological Pathways

2020 ◽  
Vol 21 (19) ◽  
pp. 7332 ◽  
Author(s):  
Ashley Hall ◽  
Sara Bandres-Ciga ◽  
Monica Diez-Fairen ◽  
John P. Quinn ◽  
Kimberley J. Billingsley
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Genetic Risk ◽  
Large Scale ◽  
Biological Pathways ◽  
Risk Scores ◽  
Potential Contribution ◽  
Genetic Profiling ◽  
Gwa Studies ◽  
Insight Into

Parkinson’s disease (PD) is a complex disorder underpinned by both environmental and genetic factors. The latter only began to be understood around two decades ago, but since then great inroads have rapidly been made into deconvoluting the genetic component of PD. In particular, recent large-scale projects such as genome-wide association (GWA) studies have provided insight into the genetic risk factors associated with genetically ‘’complex’’ PD (PD that cannot readily be attributed to single deleterious mutations). Here, we discuss the plethora of genetic information provided by PD GWA studies and how this may be utilized to generate polygenic risk scores (PRS), which may be used in the prediction of risk and trajectory of PD. We also comment on how pathway-specific genetic profiling can be used to gain insight into PD-related biological pathways, and how this may be further utilized to nominate causal PD genes and potentially druggable therapeutic targets. Finally, we outline the current limits of our understanding of PD genetics and the potential contribution of variation currently uncaptured in genetic studies, focusing here on uncatalogued structural variants.

An insight into the Phlebotomus perniciosus saliva by a proteomic approach

Acta Tropica ◽  
2012 ◽  
Vol 123 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Inés Martín-Martín ◽  
Ricardo Molina ◽  
Maribel Jiménez
Keyword(s):  
Phlebotomus Perniciosus ◽  
Proteomic Approach ◽  
Insight Into

scholarly journals Dissection of the Spindle Assembly Checkpoint by Proximity Proteomics

2020 ◽  
Author(s):  
Yenni A. Garcia ◽  
Erick F. Velasquez ◽  
Lucy W. Gao ◽  
Keith Cheung ◽  
Kevin M. Clutario ◽  
...  
Keyword(s):  
Protein Interactions ◽  
Posttranslational Modifications ◽  
Spindle Assembly Checkpoint ◽  
Protein Complexes ◽  
Spindle Assembly ◽  
Protein Protein Interactions ◽  
Proteomic Approach ◽  
Multiple Protein ◽  
Spatio Temporal ◽  
Insight Into

SUMMARYThe spindle assembly checkpoint (SAC) is critical for sensing defective microtubule-kinetochore attachments and tension across the kinetochore and functions to arrest cells in prometaphase to allow time to repair any errors prior to proceeding into anaphase. The SAC has a central role in ensuring the fidelity of chromosome segregation and its dysregulation has been linked to the development of human diseases like cancer. The establishment and maintenance of the SAC relies on multiple protein complexes that are intricately regulated in a spatial and temporal manner through posttranslational modifications like phosphorylation. Over the past few decades the SAC has been highly investigated and much has been learned about its protein constituents and the pathways and factors that regulate its activity. However, the spatio-temporal proximity associations of the core SAC components have not been explored in a systematic manner. Here, we have taken a BioID2 proximity-labeling proteomic approach to define the proximity protein environment for each of the five core SAC proteins BUB1, BUB3, BUBR1, MAD1L1, and MAD2L1 under conditions where the SAC is active in prometaphase. These five protein association maps were integrated to generate the SAC proximity protein network that contains multiple layers of information related to core SAC protein complexes, protein-protein interactions, and proximity associations. Our analysis validated many of the known SAC complexes and protein-protein interactions. Additionally, it uncovered new protein associations that lend insight into the functioning of the SAC and highlighted future areas that should be investigated to generate a comprehensive understanding of the SAC.

scholarly journals Toxic Peripheral Neuropathies: Agents and Mechanisms

2019 ◽  
Vol 48 (1) ◽  
pp. 152-173 ◽  
Author(s):  
William M. Valentine
Keyword(s):  
Protein Biosynthesis ◽  
Biological Pathways ◽  
Therapeutic Interventions ◽  
Peripheral Neuropathies ◽  
Neuronal Perikaryon ◽  
Structure Activity ◽  
Associated Lesions ◽  
Main Components ◽  
Important Form ◽  
Insight Into

Toxic peripheral neuropathies are an important form of acquired polyneuropathy produced by a variety of xenobiotics and different exposure scenarios. Delineating the mechanisms of neurotoxicants and determining the degenerative biological pathways triggered by peripheral neurotoxicants will facilitate the development of sensitive and specific biochemical-based methods for identifying neurotoxicants, designing therapeutic interventions, and developing structure–activity relationships for predicting potential neurotoxicants. This review presents an overview of the general concepts of toxic peripheral neuropathies with the goal of providing insight into why certain agents target the peripheral nervous system and produce their associated lesions. Experimental data and the main hypotheses for the mechanisms of selected agents that produce neuronopathies, axonopathies, or myelinopathies including covalent or noncovalent modifications, compromised energy or protein biosynthesis, and oxidative injury and disruption of ionic gradients across membranes are presented. The relevance of signaling between the main components of peripheral nerve, that is, glia, neuronal perikaryon, and axon, as a target for neurotoxicants and the contribution of active programmed degenerative pathways to the lesions observed in toxic peripheral neuropathies is also discussed.

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