<HashMap><database>ENA</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/001/SRR8352531/SRR8352531_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/002/SRR8352532/SRR8352532_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/009/SRR8352529/SRR8352529_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/009/SRR8352529/SRR8352529_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/000/SRR8352530/SRR8352530_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/003/SRR8352533/SRR8352533_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/002/SRR8352532/SRR8352532_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/000/SRR8352530/SRR8352530_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/003/SRR8352533/SRR8352533_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR835/001/SRR8352531/SRR8352531_1.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><center_name>Linxin lab, school of medicine, Tsinghua university</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA510753</full_dataset_link><scientific_name>Mus musculus</scientific_name><long_description>We report that the paracaspase Malt1 is required for the development and function of Treg cells. By generating Malt1 conditional knockout and protease dead mutant mice, we found Malt1-loss in Treg cells would lead to early-onset lethal autoimmune disease and the mice would die within 40 days after birth. Interestingly, mice with Treg specific inhibition of Malt1 protease activity develop spontaneous inflammatory disorders. Overall design: YFP+ Treg cells sorted from WT, cKO and cKI mice were used for RNA extraction and RNA-sequencing</long_description><repository>ENA</repository><description_synonyms>regulatory T lymphocyte, Immune Processes, Immune Responses, Malignant Neoplasm, suppressor T lymphocyte, alpha-beta regulatory T-cell, Malignancy, Process, D430033E09Rik, Neoplasms, CD4-positive, Benign Neoplasm, MLT, A630046N12, Benign Neoplasms, function, regulatory T-cell, Cancers, MLT1, Tumor, Malignant, suppressor T cell, Cell, Malignant Neoplasms, alpha-beta regulatory T-lymphocyte, suppressor T-cell, Neoplasias, suppressor T-lymphocyte, Immune Response, Immune, Treg, Benign, IMD12, regulatory T-lymphocyte, mlt1, alpha-beta regulatory T lymphocyte, Neoplasm, Response, mlt, Malignancies, CD25-positive, Immune., other neoplasm, Immune Process, Neoplasia, Cancer, Tumors</description_synonyms><name_synonyms>regulatory T lymphocyte, Immune Processes, Immune Responses, Malignant Neoplasm, suppressor T lymphocyte, alpha-beta regulatory T-cell, Malignancy, Process, D430033E09Rik, Neoplasms, CD4-positive, Benign Neoplasm, MLT, A630046N12, Benign Neoplasms, function, regulatory T-cell, Cancers, MLT1, Tumor, Malignant, suppressor T cell, Cell, Malignant Neoplasms, alpha-beta regulatory T-lymphocyte, suppressor T-cell, Neoplasias, suppressor T-lymphocyte, Immune Response, Immune, Treg, Benign, IMD12, regulatory T-lymphocyte, mlt1, alpha-beta regulatory T lymphocyte, Neoplasm, Response, mlt, Malignancies, CD25-positive, Immune., other neoplasm, Immune Process, Neoplasia, Cancer, Tumors</name_synonyms></additional><is_claimable>false</is_claimable><name>Malt1 protease is critical in maintaining function of Treg cells and may be a therapeutic target for anti-tumor immunity</name><description>Malt1 protease is critical in maintaining function of Treg cells and may be a therapeutic target for anti-tumor immunity</description><dates><last_updated>2025-09-24</last_updated><first_public>2019-01-03</first_public></dates><accession>PRJNA510753</accession><cross_references><GEO>GSE124089</GEO><taxon>10090</taxon></cross_references></HashMap>