<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/SRR247/042/SRR24756142/SRR24756142_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/045/SRR24756145/SRR24756145_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/047/SRR24756147/SRR24756147_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/045/SRR24756145/SRR24756145_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/044/SRR24756144/SRR24756144_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/042/SRR24756142/SRR24756142_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/043/SRR24756143/SRR24756143_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/046/SRR24756146/SRR24756146_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/046/SRR24756146/SRR24756146_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/047/SRR24756147/SRR24756147_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/043/SRR24756143/SRR24756143_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR247/044/SRR24756144/SRR24756144_2.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>Tongji Hospital Affiliated to Tongji University School of Medicine</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA977059</full_dataset_link><scientific_name>Mus musculus</scientific_name><long_description>Autism spectrum disorder (ASD) is a heterogeneous group of disorders with shared diagnostic phenotypes, such as reduced interest in social interaction and communication, and increased stereotyped or restricted interests and behaviors. Little is known about the involvement of alterations of glutaminase 1 (Gls1, an enzyme that catalyzes the hydrolysis of glutamine into glutamate) in the pathogenesis of ASD. To investigate the role of Gls1 in forebrain neurons , we generated conditional mouse mutants with loss of Gls1 in forebrain CamKIIα-Cre positive neurons by crossing Gls1flox/flox mice with CamKIIαcre mice. Overall design: Conditional mouse mutants with loss of Gls1 in forebrain CamKIIα-Cre positive neurons were generated by crossing Gls1flox/flox mice with CamKIIαcre mice. Mosaic homozygous Gls1 mutant (CamKIIαCre Gls1flox/flox) mice were not viable. Only mosaic heterozygous Gls1 mice (CamKIIαCre Gls1+/flox mice, referred to as Gls1_CamKIIαCre mice) and their littermate CamKIIαCre Gls1+/+ mice (referred to as control mice) were used in this study. Cells from the prefrontal cortex of both groups were isolated for Single-Nucleus RNA sequencing. Three animals were included for each group.</long_description><tag>xref:PubMed:37384529</tag><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Single-nucleus RNA sequencing of the prefrontal cortex from mice lacking glutaminase 1 in CamKIIa-positive neurons and control mice</name><description>Single-nucleus RNA sequencing of the prefrontal cortex from mice lacking glutaminase 1 in CamKIIa-positive neurons and control mice</description><dates><last_updated>2025-09-24</last_updated><first_public>2023-06-03</first_public></dates><accession>PRJNA977059</accession><cross_references><GEO>GSE233639</GEO><taxon>10090</taxon><PubMed>37384529</PubMed></cross_references></HashMap>