Polymer thin film promotes tumor spheroid formation via JAK2-STAT3 signaling primed by fibronectin-integrin 5ɑ and sustained by LMO2-LDB1 complex
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA882831 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21659059_1.fastq.gz | Fastqsanger.gz | |||
| SRR21659059_2.fastq.gz | Fastqsanger.gz | |||
| SRR21659060_1.fastq.gz | Fastqsanger.gz | |||
| SRR21659060_2.fastq.gz | Fastqsanger.gz | |||
| SRR21659061_1.fastq.gz | Fastqsanger.gz |
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Project description:LMO2 is a component of multisubunit DNA-binding transcription factor complexes that regulate gene expression in hematopoietic stem and progenitor cell development. Enforced expression of LMO2 causes leukemia by inducing hematopoietic stem cell-like features in T-cell progenitor cells, but the biochemical mechanisms of LMO2 function have not been fully elucidated. In this study we systematically dissected the LMO2/LDB1 binding interface to investigate the role of this interaction in T-cell leukemia. Alanine scanning mutagenesis of the LIM interaction domain of LDB1 revealed a discrete motif R320LITR required for LMO2 binding. Most strikingly, co-expression of full length, wild type LDB1 increased LMO2 steady state abundance, whereas co-expression of mutant proteins deficient in LMO2 binding compromised LMO2 stability. These mutant LDB1 proteins also exerted dominant negative effects on growth and transcription in diverse leukemic cell lines. Raw gene expression data on HSB-2 cells is presented here. RNAseq were performed on HSB cell lines to examine their expression patterns
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