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Single-cell RNA sequencing of the kidneys from adult Axl WT and KO mice

ABSTRACT: This study aims to delineate the effects of AXL deletion on kidney development and cellular heterogeneity by analyzing single-cell RNA transcriptomic datasets from 11-week-old male Axl wild type (WT) and heterozygous (het) knockout mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE268166 | GEO | 2025/05/30

REPOSITORIES: GEO

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RNA-seq of MMTV-Neu AXL KO tumors

Project description:AXL is activated by its ligand GAS6 and is expressed in triple-negative breast cancer cells. We report that AXL is also detected in HER2+ breast cancer specimens where its expression correlates with poor patients’ survival. Using murine models of HER2+ breast cancer, AXL, but not Gas6, was found essential for metastasis. We determined that AXL is required for intravasation, extravasation and growth at the metastatic site. AXL is expressed in HER2+ cancers displaying EMT signatures and contributes to sustain EMT in murine tumors. Interfering with AXL in patient-derived xenograft impaired TGF-β-induced cell invasion. Lastly, pharmacological inhibition of AXL decreased the metastatic burden of mice developing HER2+ breast cancer. Our data identify AXL as a potential co-therapeutic target during the treatment of HER2+ breast cancers to limit metastasis.

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RNA-seq of MMTV-Neu AXL KO tumor grafts in FVB

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RNA-seq of NIC AXL KO in hypoxia

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Opposing role of phagocytic receptors MERTK and AXL in Progranulin deficient FTD

Project description:Genetic mutations in the progranulin gene, GRN, cause frontotemporal dementia and a lysosomal storage disorder. Using single-nuclei RNA sequencing of the post-mortem brain tissue from heterozygous pathogenic granulin variant (GRN+/-) carriers we found dysregulation of microglia, phagocytosis and the phagocytic receptors MERTK and AXL. Exogenous progranulin regulated MERTK and AXL RNA expression in human microglia induced from iPSCs irrespective of GRN mutation status, without directly binding to MERTK or AXL proteins. We generated double knock-out mice and found that constitutive homozygous loss of Grn and Mertk (Grn-/-;Mertk-/-) rescued microglial disease signature while constitutive homozygous loss of Grn and Axl (Grn-/-;Axl-/-) worsened the microglial disease signature. Higher levels of AXL protein, but not MERTK protein, in the post-mortem superior temporal gyrus correlated with worse cross-sectional functional impairment (CDR sum of boxes) by both GRN+/- mutation carriers and non-carrier controls. These data explain in part the inflammation seen in GRN-FTD and are applicable to other inflammatory states in which PGRN, MERTK and AXL play regulatory roles, including cancer, sepsis, stroke, diabetes and obesity. The interaction between GRN, MERTK and AXL opens potential new therapeutic avenues to intervene on this inflammatory axis.

2025-06-30 | GSE250280 | GEO

Compare transcriptional profile of AXL knockdown cell and AXL wild type cell

Project description:We report the comparative investigation of gene expression profiles between genetic inactivation AXL cell and AXL wild type cells in two independent We found a list of AXL signaling target genes that are important for tumor invasion and angiogenesis.

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RNA-seq of NIC AXL KO in hypoxia

Project description:RNA-seq of NIC AXL KO in hypoxia

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RNA Sequencing Analysis of Nicol-Het, Nicol-KO and Ros1-KO Caput Epididymal Transcriptomes.

Project description:Purpose: The goal of this study is to detect differentially expressed genes, between Nicol +/- (Nicol-Het), Nicol-/- (Nicol-KO), and Ros1-/- (Ros1-KO) caput epididymis by RNA sequencing Methods: Caput epidiymal mRNA profiles of 14-week-old Nicol-Het, Nicol-KO, and Ros1-KO mice were generated by deep sequencing, in triplicate, using Illumina NovaSeq6000. Results: RNA-seq data identified differentially expressed transcripts. Conclusions: Our results show that the expression of many genes were downregulated in Nicol-KO caput epididymis compared with Nicol-Het one. The gene downregulation of Nicol-KO caput epididymis was similar to that of Ros1-KO one.

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Single-cell RNA sequencing of the kidneys from adult Axl WT and KO mice

Project description:Single-cell RNA sequencing of the kidneys from adult Axl WT and KO mice

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Gas6-Axl signaling drives oral regenerative wound repair

Project description:Rapid and scarless wound repair is a hallmark of the oral mucosa, yet the cellular and molecular mechanisms that enable this regeneration remain unclear. By comparing populations of oral mucosal fibroblasts (OMFs) and facial skin fibroblasts (FSFs), we have identified the mechanisms that facilitate regeneration over fibrosis. We found that OMFs utilize Growth arrest specific-6 (GAS6)-AXL signaling to suppress fibrosis-related mechanosignaling via Focal adhesion kinase (FAK). Inhibition and knockdown of AXL in the oral mucosa resulted in fibrotic wounds and increased activation of FAK. At the same time, stimulation of AXL in the facial skin yielded wounds that heal regeneratively. Rare human oral scars that resulted from repetitive injury showed decreased expression of GAS6/AXL and increased FAK. Activating AXL in repetitively injured mouse oral tissue resulted in better wound healing outcomes and reduced scarring. Together, our work demonstrates that AXL signaling is necessary for regenerative wound healing in the oral mucosa and sufficient to limit facial skin fibrosis.

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Gene expression analysis of dissociated and FDG FACS-sorted mammary glands of 16 week old nulliparous AXL +/LacZ and AXL LacZ/LacZ mice (B6.129P2-AXLtm1Dgen strain, Jackson Labs)

Project description:The receptor tyrosine kinase AXL is associated with epithelial plasticity in several solid tumors including breast cancer and AXL-targeting agents are currently in clinical trials. We hypothesized that AXL is a driver of stemness traits in cancer by co-option of a regulatory function normally reserved for stem cells. AXL-expressing cells in human mammary epithelial ducts co-expressed markers associated with multipotency, and AXL inhibition abolished colony-formation and self-maintenance activities while promoting terminal differentiation in vitro. Axl-null mice did not exhibit a strong developmental phenotype, but enrichment of Axl+ cells was required for mouse mammary gland reconstitution upon transplantation, and Axl-null mice had reduced incidence of Wnt1-driven mammary tumors. An AXL-dependent gene signature is a feature of transcriptomes in basal breast cancers, and reduced patient survival irrespective of subtype. Our interpretation is that AXL regulates access to epithelial plasticity programs in MaSCs and, when coopted, maintains acquired stemness in breast cancer cells.

2020-08-25 | GSE156662 | GEO

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