Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MMP14-wild type (WT) vs. MMP14-deficient (KO) liver mesenchymal cells derived from embryonic day (E) 16.5 mouse livers

ABSTRACT: Transcriptional profiling of systemic MMP14-KO and littermate WT mesenchymal cells in E16.5 livers. CD45-Ter119-p75NTR (NFGR)-positive liver mesenchymal cells were purified using fluorescence-activated cell sorter (FACS).

ORGANISM(S): Mus musculus

PROVIDER: GSE139517 | GEO | 2020/01/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

MMP14-wild type (WT) vs. MMP14-deficient (KO) liver mesenchymal cells derived from embryonic day (E) 16.5 mouse livers

Project description:MMP14-wild type (WT) vs. MMP14-deficient (KO) liver mesenchymal cells derived from embryonic day (E) 16.5 mouse livers

| PRJNA580020 | ENA

Expression array of stromal Mmp14-targeted mammary glands

Project description:Mammary gland branching morphogenesis is thought to depend on the mobilization of proteolytic machinery from the matrix metalloproteinase (MMP) family, namely MT1-MMP/MMP14, to drive coordinated epithelial cell invasion through the interstitial extracellular matrix, but the dominant effector has remained undefined. Unexpectedly, we find MMP14 controls postnatal mammary gland branching from the periductal stroma. Transcriptome profiling of stromal cell-targeted mammary glands was used to characterize the impact of stromal Mmp14-targeting on the growth factor and signaling cascades implicated in mammary gland morphogenesis. Transcriptome profiling of ductal networks and associated stroma was used to investigate the functional roles of MMP14 in the postnatal mammary gland stroma in an unbiased fashion.

2019-03-01 | GSE79088 | GEO

MMP14 knockdown at U87 brain tumor cells.Analyse of the genes responsible for cell division

Project description:Compared to the Scramble U87 cells, MMP14 ablation induces G2M arrest SABioscience Cell cycle platform, human genes. U87 cells were infected separately with eithr lentivirus carry on Scramble or sh RNA against human MMP14 gene.Equla amount of mRNA was isolated prior RT-PCR analyses

2013-03-19 | E-GEOD-45294 | biostudies-arrayexpress

Mmp14 is essential for circadian clock rhythmicity in fibroblasts

Project description:Membrane type I-matrix metalloproteinase (MT1-MMP/Mmp14) is an unusual MMP because it is essential for survival in mice with multiple organ systems being affected for reasons that are unclear. Here, we show that the protein (MT1-MMP) and gene (Mmp14) are under strict circadian clock control and conditional knockout in fibroblasts leads to ~16% of the proteome losing or inverting circadian rhythmicity. The result is loss of the actin cytoskeleton and cell-matrix adhesions and major imbalance of the matrisome. Lack of collagen-I monomer turnover results in excess fibril formation in the absence of Mmp14. In the absence of Mmp14, paired-like homeodomain transcription factor 2 (Pitx2) is upregulated and remains in the nucleus where it drives Plod2 expression. The overall result is accumulation of collagen fibrils and elevated pyridinoline crosslinking that renders collagen fibrils insoluble. In conclusion, Mmp14 is a master regulator of circadian rhythms affecting the actin cytoskeleton and cell microenvironment.

2023-10-31 | PXD031692 | Pride

Mmp14-Dependent Remodeling of the Pericellular-Dermal Collagen Interface Governs Fibroblast Survival

Project description:Dermal fibroblasts deposit type I collagen, the dominant extracellular matrix molecule found in skin, during early postnatal development. Coincident with this biosynthetic program, fibroblasts proteolytically remodel pericellular collagen fibrils by mobilizing the membrane-anchored matrix metalloproteinase, Mmp14. Unexpectedly, dermal fibroblasts in Mmp14-/- mice commit to a large-scale apoptotic program that leaves skin tissues replete with dying cells. A requirement for Mmp14 in dermal fibroblast survival is recapitulated in vitro when cells are embedded within, but not cultured atop, 3-dimensional hydrogels of cross-linked type I collagen. In the absence of Mmp14-dependent pericellular proteolysis, dermal fibroblasts fail to trigger β1 integrin activation and instead actuate a TGF-β1/phospho-JNK stress response that leads to apoptotic cell death in vitro as well as in vivo. Taken together, these studies identify Mmp14 as a requisite cell survival factor that maintains dermal fibroblast viability in postnatal dermal tissues.

2024-05-24 | GSE266914 | GEO

MMP14 cleaves PTH1R in the chondrocyte derived osteoblast lineage, curbing signaling intensity for proper bone anabolism

Project description:Bone homeostasis is regulated by hormones such as parathyroid hormone (PTH). While PTH can stimulate osteo-progenitor expansion and bone synthesis, how the PTH-signaling intensity in progenitors is controlled is unclear. Endochondral bone osteoblasts arise from perichondrium-derived osteoprogenitors and hypertrophic chondrocytes (HC). We found, via single-cell transcriptomics, HC descendent cells activate membrane-type 1 metalloproteinase 14 (MMP14) and the PTH pathway as they transition to osteoblasts in neonatal and adult mice. Unlike Mmp14 global knockouts, postnatal day 10 (p10) HC lineage-specific Mmp14 null mutants (Mmp14ΔHC) produce more bone. Mechanistically, MMP14 cleaves the extracellular domain of PTH1R, dampening PTH signaling, and consistent with the implied regulatory role, in Mmp14ΔHC mutants, PTH signaling is enhanced. We found HC-derived osteoblasts contribute ~50% of osteogenesis promoted by treatment with PTH 1-34 and this response was amplified in Mmp14ΔHC. MMP14 control of PTH signaling likely applies also to both HC- and non-HC-derived osteoblasts because their transcriptomes are highly similar. Our study identifies a novel paradigm of MMP14 activity-mediated modulation of PTH signaling in the osteoblast lineage, contributing new insights into bone metabolism with therapeutic significance for bone-wasting diseases.

2023-03-13 | GSE222203 | GEO

Expression array of carcinoma cell Mmp14-targeted MMTV-PyMT mammary tumors

Project description:Breast carcinoma cell invasion is thought to depend on the mobilization of the membrane-anchored matrix metalloproteinase, Mmp14/MT1-MMP, to drive the remodeling of extracellular matrix and trigger associated signaling cascades. However, the roles that this proteinase plays during breast tumor progression and invasion in vivo remain undefined. A highly penetrant syngeneic mouse model for luminal B breast cancer driven by the polyoma middle T (PyMT) antigen, in tandem with recently developed Mmp14-floxed mice and MMTV-Cre transgenics that express Cre recombinase throughout the mammary epithelial cell compartment, were used to characterize the impact of conditional Mmp14-targeting on breast carcinoma cell invasion programs in vivo. Transcriptome profiling of intact MMTV-PyMT carcinoma tumors was used to investigate the functional roles of carcinoma cell-derived MT1-MMP in MMTV-PyMT tumor progression and invasion in an unbiased fashion

2018-12-01 | GSE118466 | GEO

TGF-β signaling plays an essential role in the lineage specification of mesenchymal stem/progenitor cells in fetal bone marrow

Project description:TGF-β regulates fetale bone marrow niche emergence. Abrogating TGF-β signaling in mesenchymal cells during development results in a marked expansion of adipocytes and CAR cells in the bone marrow, while osteoblasts are reduced. RNA expression data from Osx-Cre targeted mesenchymal stromal cells obtained from E16.5 mouse hindlimbs of transgenic mice lacking Tgfbr2 in mesenchymal stromal cells or littermate controls.

2019-05-15 | GSE131219 | GEO

MMP14 knockdown at U87 brain tumor cells.Analyse of the genes responsible for cell division

Project description:Compared to the Scramble U87 cells, MMP14 ablation induces G2M arrest

2013-03-19 | GSE45294 | GEO

Expression array of mammary epithelial cells isolated from epithelial Mmp14-targeted mammary glands

Project description:Mammary gland branching morphogenesis is thought to relie on the mobilization of the membrane-anchored matrix metalloproteinase, Mmp14/MT1-MMP, to drive mammary epithelial invasion by remodeling the extracellular matrix and triggering associated signaling cascades. However, the roles that this proteinase plays during postnatal mammary gland development in vivo remain undefined. A mammary gland branching program that occurs during the first 4 weeks of postnatal mouse development, in tandem with recently developed Mmp14-floxed mice and MMTV-Cre transgenics that express Cre recombinase throughout the mammary epithelial cell compartment, were used to characterize the impact of deleting epithelial cell Mmp14 on mammary gland morphogenesis. Transcriptome profiling of mammary epithelial cells was used to investigate the functional roles of MT1-MMP in the postnatal mammary epithelial cell compartment in an unbiased fashion

2018-12-01 | GSE118465 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data