Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Short Tandem Repeats - Targeted-Sequencing of human cells for Lineage tracing

ABSTRACT: Short Tandem Repeats - Targeted-Sequencing of human cells for Lineage tracing

PROVIDER: PRJEB25050 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Short tandem repeats are important contributors to silencer elements in T cells

Project description:Short tandem repeats are important contributors to silencer elements in T cells

2023-02-28 | GSE219157 | GEO

Short Tandem Repeats - Targeted-Sequencing of human cells for Lineage tracing

Project description:Raw sequencing data used in the paper \"A biological-computational cell lineage discovery platform based on duplex MIPs\" (doi: https://doi.org/10.1101/191296) involving single cells from the YUCLAT melanoma patient and DU145 cell line which cultured in standart condition as recommend. The single cells were prepared by CellCellector for DU145 and FACS for YUCLAT, amplified by RepliG WGA kit . Targeting sequencing library is cronstructed with duplex Molecular Inversion Probes wtih the protocol as described in the paper. Illumina NextSeq is used to sequence these libraries.

2018-03-01 | E-MTAB-6411 | biostudies-arrayexpress

Short tandem repeats susceptible to pathogenic instability linked to chromatin domain disruption

Project description:Short tandem repeats susceptible to pathogenic instability linked to chromatin domain disruption

| PRJNA436095 | ENA

DNA polymerase stalling at structured DNA predicts the stability of short tandem repeats

Project description:DNA polymerase stalling at structured DNA predicts the stability of short tandem repeats

| PRJNA603735 | ENA

DNA polymerase stalling at structured DNA predicts the stability of short tandem repeats

Project description:Short tandem repeats (STRs) significantly contribute to de novo mutagenesis, driving phenotypic diversity and genetic disease. Although highly diverse, their low complexity and repetitive nature induces DNA polymerase slippage and stalling, leading to length variation and base substitutions. However, the characterisation of DNA synthesis through STR loci has been restricted to a handful of selected sequences, limiting our broader understanding of their evolutionary behaviour. In order to understand the interplay between the ability of a given STR to impair DNA synthesis and its genomic stability, we developed a high-throughput polymerase extension assay that allows monitoring the kinetics of DNA synthesis at all STR permutations in different lengths in parallel. We have used the assay to map at single-nucleotide resolution the movement of a prototypical A-family replicative DNA polymerase (T7 DNA polymerase) through the repeats over time. From this data we can infer the secondary structure adopted by a given STR from the precise manner in which it stalls polymerase and link this to slippage and point mutation during DNA synthesis.

2020-07-27 | GSE144458 | GEO

Short tandem repeats susceptible to pathogenic instability linked to chromatin domain disruption

Project description:More than 25 inherited human disorders are caused by the unstable expansion of repetitive DNA sequences termed short tandem repeats (STRs). A fundamental unresolved question is why some STRs are susceptible to pathologic expansion, whereas thousands of repeat tracts across the human genome are relatively stable. Here, we discover that nearly all disease-associated STRs (daSTRs) are located at boundaries demarcating 3D chromatin domains. We identify a subset of boundaries with markedly higher CpG island density compared to the rest of the genome. daSTRs specifically localize to ultra-high-density CpG island boundaries, suggesting they might be hotspots for epigenetic misregulation or topological disruption upon STR expansion. Fragile X Syndrome (FXS) patients exhibit severe boundary disruption in a manner that correlates with local loss of CTCF occupancy and the degree of FMR1 silencing. Our data uncover higher-order chromatin architecture as a new dimension in understanding repeat expansion disorders.

2018-08-29 | GSE111170 | GEO

Switch tandem repeats influence the choice of the alternative end-joining pathway in class switch recombination

Project description:Switch tandem repeats influence the choice of the alternative end-joining pathway in class switch recombination

2022-05-11 | GSE174296 | GEO

Retrospective cell lineage reconstruction in humans by using short tandem repeats.

Project description: Not available

| S-EPMC8313865 | biostudies-literature

Cell-type specific dysregulation of RNA alternative splicing in short tandem repeat mouse knockin models of myotonic dystrophy

Project description:Short tandem repeats (STRs) are prone to expansion mutations that cause multiple hereditary neurological and neuromuscular diseases. To study pathomechanisms using mouse models that recapitulate the tissue specificity and developmental timing of an STR expansion gene, we used rolling circle amplification and CRISPR/Cas9-mediated genome editing to generate Dmpk CTG expansion (CTGexp) knockin models of myotonic dystrophy type 1 (DM1). We demonstrate that skeletal muscle myoblasts and brain choroid plexus epithelial cells are particularly susceptible to Dmpk CTGexp mutations and RNA mis-splicing. Our results implicate dysregulation of muscle regeneration and cerebrospinal fluid homeostasis as early pathogenic events in DM1.

2019-11-15 | GSE137494 | GEO

Short Tandem Repeat Typing for Candida krusei

Project description:Development of a multiplex PCR short tandem repeat typing scheme for Candida krusei

| PRJEB49054 | ENA