Similar Datasets
Project description:Effect of Ly6d overexpression on the mechanism of MASLD
| PRJNA1283206 | ENA
Project description:To investigate the regulatory function of LY6D in NAFLD, we established a LY6D-overexpressing L02 cell line treated with FFAs.
2026-06-20 | GSE300257 | GEO
Project description:We performed gene expression microarray comparing Ly6D- CLPs isolated from OcnCre;iDTR control and mutant mice by flow cytometry. Ly6D- CLPs were isolated from the bone marrow of OcnCre;iDTR control or mutant mice by flow cytometry and subjected to Affymetrix microarray comparison of gene expression. Markers used to define Ly6D- CLP by flow cytometry was: LineageLo, cKit+, Sca+, CD127+, Thy1.2-, Ly6D-
2015-04-10 | E-GEOD-66102 | biostudies-arrayexpress
Project description:In the normal prostate, most basal and some luminal cells are castration-resistant (CR). The identity of these CR cells and their relation to CR prostate cancer are unresolved. We compared single-cell expression profiles of prostate cells sorted from hormonally naïve (HN) and castrated mice. We found both basal and luminal-localized cells, particularly the latter, were molecularly heterogeneous. CR luminal cells and a subset of HN luminal cells exhibited a similar “intermediate” expression pattern, including high-level expression of multiple prostate stem/progenitor marker genes and androgen receptor gene. We validated LY6D as a marker linking CR luminal cells to luminal progenitors. LY6D+ prostate cells, including LY6D+ luminal cells, were enriched for organoid-forming potential regardless of the presence or absence of androgen. Krt8-based lineage-tracing revealed that LY6D+ CR luminal cells produced LY6D- normal luminal cells upon regeneration, but LY6D+ luminal cancer cells under PTEN-deficiency. Furthermore, prostate cancers originating from CR luminal cells (LY6D+) exhibited a more advanced phenotype than those from HN luminal cells (LY6D+ or LY6D-). Lastly, LY6D amplification/upregulation appear associated with advanced prostate cancer in patient samples. Together, our studies demonstrate LY6D as a novel progenitor marker predictive of lethal CR disease.
2018-12-21 | GSE92473 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy driven by oncogenic KRAS and inflammation-induced cellular heterogeneity, yet the mechanisms underlying tumor-initiating cells (TICs) emergence and maintenance remain unclear. Our study establishes LY6D as a marker of persistent TICs that orchestrate pancreatic cancer progression across all disease stages. Single-cell RNA sequencing of inflammation-driven PDAC models reveals that LY6D+ TICs specifically originate from KRAS-mutant acinar-to-ductal metaplasia (ADM) lesions under inflammatory conditions, maintaining conserved stemness properties and exhibiting a distinctive oxidative phosphorylation (OXPHOS) dependency throughout tumor evolution. Moreover, genetic ablation of Ly6d in KrasG12D pancreata delays tumorigenesis, while forced Ly6d expression enhances tumorigenic potential and metastatic capability. Mechanistically, LY6D-despite lacking intracellular domains-scaffolds lipid raft-associated kinase networks and FOSL1-dependent epigenetic reprogramming to establish a stable pro-tumorigenic state. Clinically, LY6D+ cells are enriched in human PDAC and exhibit conserved stemness and epithelial-mesenchymal transition (EMT) properties. Strikingly, LY6D expression levels demonstrate PDAC-restricted prognostic power. Our work defines LY6D as pan-stage TICs marker linking cellular plasticity to PDAC initiation and progression, offering new avenues for early detection and interception of this lethal ma
2026-04-09 | GSE313383 | GEO
Project description:Effect of overexpression of LY6D on gene expression in L02 hepatocytes
| PRJNA1279973 | ENA
Project description:The E-protein transcription factors E2A and HEB play important roles at several stages of hematopoiesis. However, the exact mechanism for theire action and the main targets in the LY6D negative common lymphoid progentior (CLP) compartment remains unknown. By adressing this question, we will gain important infromation regarding the early events leading to B-cell specification. FACS sorted LY6D negative common lymphoid progenitors from WT, HEB-KO and E2A-KO mice were subjected to RNA extraction and hybridization on Affymetrix microarrays. At least two independent sorts were performed per genotype. During each sort, cells were pooled from several bone marrows.
2011-11-22 | E-GEOD-27402 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy driven by oncogenic KRAS and inflammation-induced cellular heterogeneity, yet the mechanisms underlying tumor-initiating cells (TICs) emergence and maintenance remain unclear. Our study establishes LY6D as a marker of persistent TICs that orchestrate pancreatic cancer progression across all disease stages. Single-cell RNA sequencing of inflammation-driven PDAC models reveals that LY6D+ TICs specifically originate from KRAS-mutant acinar-to-ductal metaplasia (ADM) lesions under inflammatory conditions, maintaining conserved stemness properties and exhibiting a distinctive oxidative phosphorylation (OXPHOS) dependency throughout tumor evolution. Moreover, genetic ablation of Ly6d in KrasG12D pancreata delays tumorigenesis, while forced Ly6d expression enhances tumorigenic potential and metastatic capability. Mechanistically, LY6D-despite lacking intracellular domains-scaffolds lipid raft-associated kinase networks and FOSL1-dependent epigenetic reprogramming to establish a stable pro-tumorigenic state. Clinically, LY6D+ cells are enriched in human PDAC and exhibit conserved stemness and epithelial-mesenchymal transition (EMT) properties. Strikingly, LY6D expression levels demonstrate PDAC-restricted prognostic power. Our work defines LY6D as pan-stage TICs marker linking cellular plasticity to PDAC initiation and progression, offering new avenues for early detection and interception of this lethal malignancy.
2026-04-09 | GSE299488 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy driven by oncogenic KRAS and inflammation-induced cellular heterogeneity, yet the mechanisms underlying tumor-initiating cells (TICs) emergence and maintenance remain unclear. Our study establishes LY6D as a marker of persistent TICs that orchestrate pancreatic cancer progression across all disease stages. Single-cell RNA sequencing of inflammation-driven PDAC models reveals that LY6D+ TICs specifically originate from KRAS-mutant acinar-to-ductal metaplasia (ADM) lesions under inflammatory conditions, maintaining conserved stemness properties and exhibiting a distinctive oxidative phosphorylation (OXPHOS) dependency throughout tumor evolution. Moreover, genetic ablation of Ly6d in KrasG12D pancreata delays tumorigenesis, while forced Ly6d expression enhances tumorigenic potential and metastatic capability. Mechanistically, LY6D-despite lacking intracellular domains-scaffolds lipid raft-associated kinase networks and FOSL1-dependent epigenetic reprogramming to establish a stable pro-tumorigenic state. Clinically, LY6D+ cells are enriched in human PDAC and exhibit conserved stemness and epithelial-mesenchymal transition (EMT) properties. Strikingly, LY6D expression levels demonstrate PDAC-restricted prognostic power. Our work defines LY6D as pan-stage TICs marker linking cellular plasticity to PDAC initiation and progression, offering new avenues for early detection and interception of this lethal malignancy.
2026-04-09 | GSE299487 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy driven by oncogenic KRAS and inflammation-induced cellular heterogeneity, yet the mechanisms underlying tumor-initiating cells (TICs) emergence and maintenance remain unclear. Our study establishes LY6D as a marker of persistent TICs that orchestrate pancreatic cancer progression across all disease stages. Single-cell RNA sequencing of inflammation-driven PDAC models reveals that LY6D+ TICs specifically originate from KRAS-mutant acinar-to-ductal metaplasia (ADM) lesions under inflammatory conditions, maintaining conserved stemness properties and exhibiting a distinctive oxidative phosphorylation (OXPHOS) dependency throughout tumor evolution. Moreover, genetic ablation of Ly6d in KrasG12D pancreata delays tumorigenesis, while forced Ly6d expression enhances tumorigenic potential and metastatic capability. Mechanistically, LY6D-despite lacking intracellular domains-scaffolds lipid raft-associated kinase networks and FOSL1-dependent epigenetic reprogramming to establish a stable pro-tumorigenic state. Clinically, LY6D+ cells are enriched in human PDAC and exhibit conserved stemness and epithelial-mesenchymal transition (EMT) properties. Strikingly, LY6D expression levels demonstrate PDAC-restricted prognostic power. Our work defines LY6D as pan-stage TICs marker linking cellular plasticity to PDAC initiation and progression, offering new avenues for early detection and interception of this lethal malignancy.
2026-04-09 | GSE299489 | GEO