Asset Details
MbrlCatalogueTitleDetail
Do you wish to reserve the book?
Evidence for enhancer activity in intron 1 of TNFRSF1A using CRISPR/Cas9 in human induced pluripotent stem cell-derived macrophages
by
Palmer, Madeleine H.
, Davies, Ben
, Cowley, Sally A.
, Brown, Andrew C.
, Tay, Chwen
, Migliorini, Gabriele
, Burnham, Katie L.
, Osgood, Julie A.
, Mielczarek, Olga
, Zhang, Ping
, Knight, Julian C.
in
631/208/200
/ 692/308/2056
/ Ankylosing spondylitis
/ Autoimmune diseases
/ Cell Differentiation
/ Chromatin
/ Cloning
/ CRISPR
/ CRISPR-Cas Systems
/ Enhancer Elements, Genetic
/ Epigenetics
/ Epigenomics
/ Functional genomics
/ Gene Editing
/ Gene expression
/ Gene Expression Regulation
/ Gene regulation
/ Genetic diversity
/ Genetic variance
/ Genome editing
/ Genome-wide association studies
/ Genome-Wide Association Study
/ Genomics
/ Humanities and Social Sciences
/ Humans
/ Immunoprecipitation
/ Induced Pluripotent Stem Cells - cytology
/ Induced Pluripotent Stem Cells - metabolism
/ Inflammatory bowel diseases
/ Introns - genetics
/ Macrophages
/ Macrophages - cytology
/ Macrophages - metabolism
/ multidisciplinary
/ Multiple sclerosis
/ Pluripotency
/ Receptors, Tumor Necrosis Factor, Type I - genetics
/ Regulatory sequences
/ Science
/ Science (multidisciplinary)
/ Stem cells
/ Therapeutic targets
/ TNF inhibitors
/ TNFRSF1A
/ Transcription factors
/ Transcriptomics
/ Transposase
/ Tumor necrosis factor-TNF
2025
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
You are currently in the queue to collect this book. You will be notified once it is your turn to collect the book.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Evidence for enhancer activity in intron 1 of TNFRSF1A using CRISPR/Cas9 in human induced pluripotent stem cell-derived macrophages
by
Palmer, Madeleine H.
, Davies, Ben
, Cowley, Sally A.
, Brown, Andrew C.
, Tay, Chwen
, Migliorini, Gabriele
, Burnham, Katie L.
, Osgood, Julie A.
, Mielczarek, Olga
, Zhang, Ping
, Knight, Julian C.
in
631/208/200
/ 692/308/2056
/ Ankylosing spondylitis
/ Autoimmune diseases
/ Cell Differentiation
/ Chromatin
/ Cloning
/ CRISPR
/ CRISPR-Cas Systems
/ Enhancer Elements, Genetic
/ Epigenetics
/ Epigenomics
/ Functional genomics
/ Gene Editing
/ Gene expression
/ Gene Expression Regulation
/ Gene regulation
/ Genetic diversity
/ Genetic variance
/ Genome editing
/ Genome-wide association studies
/ Genome-Wide Association Study
/ Genomics
/ Humanities and Social Sciences
/ Humans
/ Immunoprecipitation
/ Induced Pluripotent Stem Cells - cytology
/ Induced Pluripotent Stem Cells - metabolism
/ Inflammatory bowel diseases
/ Introns - genetics
/ Macrophages
/ Macrophages - cytology
/ Macrophages - metabolism
/ multidisciplinary
/ Multiple sclerosis
/ Pluripotency
/ Receptors, Tumor Necrosis Factor, Type I - genetics
/ Regulatory sequences
/ Science
/ Science (multidisciplinary)
/ Stem cells
/ Therapeutic targets
/ TNF inhibitors
/ TNFRSF1A
/ Transcription factors
/ Transcriptomics
/ Transposase
/ Tumor necrosis factor-TNF
2025
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Evidence for enhancer activity in intron 1 of TNFRSF1A using CRISPR/Cas9 in human induced pluripotent stem cell-derived macrophages
by
Palmer, Madeleine H.
, Davies, Ben
, Cowley, Sally A.
, Brown, Andrew C.
, Tay, Chwen
, Migliorini, Gabriele
, Burnham, Katie L.
, Osgood, Julie A.
, Mielczarek, Olga
, Zhang, Ping
, Knight, Julian C.
in
631/208/200
/ 692/308/2056
/ Ankylosing spondylitis
/ Autoimmune diseases
/ Cell Differentiation
/ Chromatin
/ Cloning
/ CRISPR
/ CRISPR-Cas Systems
/ Enhancer Elements, Genetic
/ Epigenetics
/ Epigenomics
/ Functional genomics
/ Gene Editing
/ Gene expression
/ Gene Expression Regulation
/ Gene regulation
/ Genetic diversity
/ Genetic variance
/ Genome editing
/ Genome-wide association studies
/ Genome-Wide Association Study
/ Genomics
/ Humanities and Social Sciences
/ Humans
/ Immunoprecipitation
/ Induced Pluripotent Stem Cells - cytology
/ Induced Pluripotent Stem Cells - metabolism
/ Inflammatory bowel diseases
/ Introns - genetics
/ Macrophages
/ Macrophages - cytology
/ Macrophages - metabolism
/ multidisciplinary
/ Multiple sclerosis
/ Pluripotency
/ Receptors, Tumor Necrosis Factor, Type I - genetics
/ Regulatory sequences
/ Science
/ Science (multidisciplinary)
/ Stem cells
/ Therapeutic targets
/ TNF inhibitors
/ TNFRSF1A
/ Transcription factors
/ Transcriptomics
/ Transposase
/ Tumor necrosis factor-TNF
2025
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Evidence for enhancer activity in intron 1 of TNFRSF1A using CRISPR/Cas9 in human induced pluripotent stem cell-derived macrophages
Journal Article
Evidence for enhancer activity in intron 1 of TNFRSF1A using CRISPR/Cas9 in human induced pluripotent stem cell-derived macrophages
2025
Request Book From Autostore
and Choose the Collection Method
Overview
TNFα is a common drug target in the treatment of autoimmune diseases, with pro-inflammatory functions that are primarily mediated through its receptor, TNFRSF1A.
TNFRSF1A
has been genetically associated with many immune-mediated diseases including ankylosing spondylitis, multiple sclerosis, and inflammatory bowel disease. Many of the genetic variants within or near
TNFRSF1A
that have been associated with disease through genome-wide association studies (GWAS) lie in non-coding regions of the genome. Understanding the functional consequences of these genetic variants is limited by incomplete understanding of
TNFRSF1A
gene regulation, including for specific cellular contexts relevant to inflammation and immunity such as macrophages. This work used CRISPR/Cas9 in human induced pluripotent stem cells followed by differentiation into macrophages to investigate putative regulatory elements in the
TNFRSF1A
gene locus. Through gene editing, with functional genomic readouts including the assay for transposase-accessible chromatin using sequencing (ATAC-Seq), chromatin immunoprecipitation with sequencing (ChIP-Seq), and RNA-Seq to assess the consequences of these edits, we present evidence for an enhancer of
TNFRSF1A
contained within an intron of the gene. Understanding gene regulation and the genomic context in which GWAS variants lie could bring us closer to deconvoluting the genetic basis of common disease aetiology and uncover effective drug targets.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ Cloning
/ CRISPR
/ Genome-wide association studies
/ Genome-Wide Association Study
/ Genomics
/ Humanities and Social Sciences
/ Humans
/ Induced Pluripotent Stem Cells - cytology
/ Induced Pluripotent Stem Cells - metabolism
/ Receptors, Tumor Necrosis Factor, Type I - genetics
/ Science
/ TNFRSF1A
This website uses cookies to ensure you get the best experience on our website.