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Thymic T-cell progenitor development is supported by membrane bound Kit ligand provided by a combined vascular endothelial and epithelial niche.

ABSTRACT: Gene expression analysis of purified KitL-tomato+ and KitL-tomato- thymic vascular endothelial cells, cortical and medullary thymic epithelial cells from 5 weeks old male kitL-tomato reporter mice

ORGANISM(S): Mus musculus

PROVIDER: GSE62741 | GEO | 2016/01/18

SECONDARY ACCESSION(S): PRJNA265043

REPOSITORIES: GEO

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Thymic T-cell progenitor development is supported by membrane bound Kit ligand provided by a combined vascular endothelial and epithelial niche.

Project description:Gene expression analysis of purified KitL-tomato+ and KitL-tomato- thymic vascular endothelial cells, cortical and medullary thymic epithelial cells from 5 weeks old male kitL-tomato reporter mice Differentially expressed genes analysis of thymic stromal cells

2016-01-18 | E-GEOD-62741 | biostudies-arrayexpress

Bi-directional signaling by membrane-bound KitL induces proliferation and co-ordinates thymic endothelial cell and thymocyte expansion

Project description:The ligand for the c-Kit receptor, KitL, exists as a membrane-associated (mKitL) and a soluble form (sKitL). KitL functions outside c-Kit activation have not been identified. We show that co-culture of c-Kit– and mKitL–expressing NIH3T3 cells results in signaling through mKitL: c-Kit–bound mKitL recruits calcium-modulating cyclophilin ligand (CAML) to selectively activate Akt, leading to CREB phosphorylation, mTOR pathway activation, and increased cell proliferation. Activation of mKitL in thymic vascular endothelial cells (VECs) induces mKitL- and Akt-dependent proliferation, and genetic ablation of mKitL in thymic VECs blocks their c-Kit responsiveness and proliferation during neonatal thymic expansion. Therefore, mKitL–c-Kit form a bi-directional signaling complex that acts in the developing thymus to coordinate thymic VEC and early thymic progenitor (ETP) expansion by simultaneously promoting ETP survival and VEC proliferation. This mechanism may be relevant to both normal tissues and malignant tumors that depend on KitL–c-Kit signaling for their proliferation.

2018-11-21 | PXD011061 | Pride

Comparison of RelB-/- and RelB+/- thymi

Project description:Thymic medullary epithelial cell (mTEC) expression of the autoimmune regulator AIRE, and of tissue-specific antigens, is controlled by members of the non-canonical NF-kB signalling pathway, including RelB and NF-kB2. Of the genes in this pathway, RelB-/- mice develop a particularly severe multi-organ autoimmune syndrome, resembling Foxp3-deficiency. RelB-/- mice have medullary atrophy and few mTECs but the mechanism is unknown. We show that RelB is required for expression of medullary chemokines and mTEC AIRE, selection of a diverse peripheral T cell repertoire, and for peripheral Foxp3+ Treg function. VÎ² families of T cells infiltrating diseased peripheral organs and thymic Treg were similarly skewed. Surprisingly, medullary atrophy results from intra-thymic granulocyte infiltration, consequent upon the Th2-mediated autoimmune disease. Dominant tolerance corrects thymic inflammatory disease and loss of thymic function. We demonstrate a reversible RelB-dependent inflammatory mechanism for loss of central tolerance associated with medullary atrophy. Thymi from 4 RelB+/- mice and 3 RelB-/- mice were profiled by microarays

2012-12-27 | E-GEOD-43154 | biostudies-arrayexpress

Comparison of RelB-/- and RelB+/- thymi

Project description:Thymic medullary epithelial cell (mTEC) expression of the autoimmune regulator AIRE, and of tissue-specific antigens, is controlled by members of the non-canonical NF-kB signalling pathway, including RelB and NF-kB2. Of the genes in this pathway, RelB-/- mice develop a particularly severe multi-organ autoimmune syndrome, resembling Foxp3-deficiency. RelB-/- mice have medullary atrophy and few mTECs but the mechanism is unknown. We show that RelB is required for expression of medullary chemokines and mTEC AIRE, selection of a diverse peripheral T cell repertoire, and for peripheral Foxp3+ Treg function. Vβ families of T cells infiltrating diseased peripheral organs and thymic Treg were similarly skewed. Surprisingly, medullary atrophy results from intra-thymic granulocyte infiltration, consequent upon the Th2-mediated autoimmune disease. Dominant tolerance corrects thymic inflammatory disease and loss of thymic function. We demonstrate a reversible RelB-dependent inflammatory mechanism for loss of central tolerance associated with medullary atrophy.

2012-12-27 | GSE43154 | GEO

Bi-directional c-Kit–mKitL signalling promotes tumour endothelial cell differentiation and triple-negative breast cancer progression

Project description:Transcriptomic analysis of lineage traced KitL+ endothelial cells from naive, small and large tumour bearing mammary gland tissue

2021-01-31 | GSE154000 | GEO

ATAC-seq profiling of medullary thymic epithelial cells from wildtype and Kat7-knockout mice

Project description:Thymic epithelial cells govern thymic T lymphocyte differentiation and selection. Medullary TECs (mTECs) facilitate the negative selection of self-reactive thymocytes and the differentiation of FOXP3+ regulatory T cells. Medullary TECs are also distinctive for their “promiscuous” gene expression, transcribing thousands of peripheral tissue genes (PTG) that are otherwise only expressed highly in one or two other organs. Much of this PTG expression by mTECs is controlled by the autoimmune regulator, AIRE. To probe the mechanism by which KAT7 promotes AIRE function, we performed ATAC-seq to compare chromatin accessibility in MHCII-high medullary thymic epithelial cells from Kat7-knockout and wildtype mice.

2021-12-21 | GSE188868 | GEO

Using supported bilayers to study the spatiotemporal organization of membrane-bound proteins.

Project description:Cell division in prokaryotes and eukaryotes is commonly initiated by the well-controlled binding of proteins to the cytoplasmic side of the cell membrane. However, a precise characterization of the spatiotemporal dynamics of membrane-bound proteins is often difficult to achieve in vivo. Here, we present protocols for the use of supported lipid bilayers to rebuild the cytokinetic machineries of cells with greatly different dimensions: the bacterium Escherichia coli and eggs of the vertebrate Xenopus laevis. Combined with total internal reflection fluorescence microscopy, these experimental setups allow for precise quantitative analyses of membrane-bound proteins. The protocols described to obtain glass-supported membranes from bacterial and vertebrate lipids can be used as starting points for other reconstitution experiments. We believe that similar biochemical assays will be instrumental to study the biochemistry and biophysics underlying a variety of complex cellular tasks, such as signaling, vesicle trafficking, and cell motility.

| S-EPMC4578691 | biostudies-literature

Gene Expression Data from Adult and Embryo Thymic Epithelial Cells (TEC)

Project description:We used Affymetrix microarrays to understand the genome wide differences in Adult and fetal cortical thymic epithelial cells (cTEC) and medullary thymic epithelial cells (mTEC)

2017-02-10 | GSE81433 | GEO

pMD-Membrane: A Method for Ligand Binding Site Identification in Membrane-Bound Proteins.

Project description:Probe-based or mixed solvent molecular dynamics simulation is a useful approach for the identification and characterization of druggable sites in drug targets. However, thus far the method has been applied only to soluble proteins. A major reason for this is the potential effect of the probe molecules on membrane structure. We have developed a technique to overcome this limitation that entails modification of force field parameters to reduce a few pairwise non-bonded interactions between selected atoms of the probe molecules and bilayer lipids. We used the resulting technique, termed pMD-membrane, to identify allosteric ligand binding sites on the G12D and G13D oncogenic mutants of the K-Ras protein bound to a negatively charged lipid bilayer. In addition, we show that differences in probe occupancy can be used to quantify changes in the accessibility of druggable sites due to conformational changes induced by membrane binding or mutation.

| S-EPMC4623977 | biostudies-literature

Measuring microtubule binding kinetics of membrane-bound kinesin motors using supported lipid bilayers.

Project description:Membrane-bound cargos in cells are generally transported by multiple kinesin motors. Quantifying the bimolecular on-rate of motors for their microtubule track is important for understanding of multi-motor transport but is complicated by diffusion of the motors in the plane of the lipid bilayer. Here, we describe a method to measure the kinesin on-rate that uses a modified microtubule gliding assay performed on a supported lipid bilayer and detects motor binding by a local increase in fluorescence. For complete details on the use and execution of this protocol, please refer to Jiang et al. (2019).

| S-EPMC8339383 | biostudies-literature

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