Transcriptional profiles of Sox4 cKO, Sox11 cKO, and Sox4/11 dcKO mouse keratinocytes
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PROVIDER: PRJNA494646 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of Sox4cKO, Sox11cKO, or Sox4/11dcKO mouse keratinocytes as compared to their wild-type control keratinocytes, isolated from gender matched neonatal pairs. Goal was to identify the genes differentially expresssed in the conditional knockout keratinocytes vs the wild-type control.
2018-10-05 | GSE120827 | GEO
Project description:Transcriptional profiles of Sox4 cKO, Sox11 cKO, and Sox4/11 dcKO mouse epidermis at E16
| PRJNA494647 | ENA
Project description:Transcriptional profiling of mouse E16 epidermis deficient of Sox4, Sox11, or both as compared to gender matched wild type littermate controls. Goal was to identify the genes differentially expresssed in the conditional knockout epidermis vs the wild-type control epidermis.
2018-10-05 | GSE120826 | GEO
Project description:Tissue injury induces changes in cellular identity, but the underlying molecular mechanisms remain obscure. Here, we show that upon damage, epidermal cells at the wound edge convert to an embryonic-like state, altering particularly the cytoskeletal/extracellular matrix (ECM) components and differentiation program. We show that SOX11 and its closest relative SOX4 dictate embryonic epidermal state, regulating genes involved in epidermal development as well as cytoskeletal/ECM organization. Correspondingly, postnatal induction of Sox11 represses epidermal terminal differentiation while deficiency of Sox11 and Sox4 accelerates differentiation and dramatically impairs cell motility and re-epithelialization. Amongst the embryonic genes reactivated at the wound edge, we identify fascin actin-bundling protein 1 (FSCN1) as a critical direct target of SOX11 and SOX4 regulating cell migration. Our study identifies the reactivated embryonic gene program during wound repair and demonstrates that SOX11 and SOX4 play a key part in this process
2019-07-13 | GSE120773 | GEO
Project description:The early retinal progenitor-expressed gene Sox11 regulates the timing of the differentiation of retinal cells. Sry-related HMG box (Sox) proteins play diverse and critical roles in a variety of morphogenetic processes during embryonic development. Sox11 and Sox4 are members of the SoxC subtype, and we found that Sox11 was strongly expressed in early retinal progenitor cells, and that when expression of Sox11 subsided around birth, Sox4 expression began. To analyze the role of Sox11 and Sox4 in retinal development, we perturbed their expression pattern by expressing them ectopically in retinal explant culture. Overexpression of Sox11 or Sox4 in retinal progenitors resulted in similar phenotypes, that is, increased cone cells and decreased Muller glia. Sox11-knockout retinas showed delayed onset and progress of differentiation of early-born retinal cells during the embryonic period. After birth, retinal differentiation took place relatively normally, probably because of the redundant activity of Sox4, which starts to differentiate around birth. Neither overexpression nor loss-of-function analysis gave any evidence that Sox11 and Sox4 directly regulate transcription of genes critical to early-born retinal cells. However, histone H3 acetylation status of the early neurogenic genes was lowered in knockout retinas, suggesting that Sox11 regulates the timing of differentiation in early-born retinas by creating an epigenetic state that helps to establish the competency to differentiate. We also found that the unique expression patterns of Sox11 and Sox4 may be achieved by the Notch signaling pathway and by epigenetic regulation. Taking our findings together, we propose that the precise regulation of Sox11 and Sox4 expression during retinogenesis by multiple mechanisms leads to the fine adjustment of retinal differentiation. To delineate the molecular mechanisms underlying the retinal action of Sox11, we performed microarray analysis of E18 retinas from wild-type and Sox11 knockout mice. Total RNA was obtained from each one retina of Sox11 knockout and wild-type littermate embryos at E18.
2012-12-28 | E-GEOD-43089 | biostudies-arrayexpress
Project description:The early retinal progenitor-expressed gene Sox11 regulates the timing of the differentiation of retinal cells. Sry-related HMG box (Sox) proteins play diverse and critical roles in a variety of morphogenetic processes during embryonic development. Sox11 and Sox4 are members of the SoxC subtype, and we found that Sox11 was strongly expressed in early retinal progenitor cells, and that when expression of Sox11 subsided around birth, Sox4 expression began. To analyze the role of Sox11 and Sox4 in retinal development, we perturbed their expression pattern by expressing them ectopically in retinal explant culture. Overexpression of Sox11 or Sox4 in retinal progenitors resulted in similar phenotypes, that is, increased cone cells and decreased Muller glia. Sox11-knockout retinas showed delayed onset and progress of differentiation of early-born retinal cells during the embryonic period. After birth, retinal differentiation took place relatively normally, probably because of the redundant activity of Sox4, which starts to differentiate around birth. Neither overexpression nor loss-of-function analysis gave any evidence that Sox11 and Sox4 directly regulate transcription of genes critical to early-born retinal cells. However, histone H3 acetylation status of the early neurogenic genes was lowered in knockout retinas, suggesting that Sox11 regulates the timing of differentiation in early-born retinas by creating an epigenetic state that helps to establish the competency to differentiate. We also found that the unique expression patterns of Sox11 and Sox4 may be achieved by the Notch signaling pathway and by epigenetic regulation. Taking our findings together, we propose that the precise regulation of Sox11 and Sox4 expression during retinogenesis by multiple mechanisms leads to the fine adjustment of retinal differentiation.
2012-12-28 | GSE43089 | GEO
Project description:Sox4 is a transcription factor expressed during embryonic development and some adult tissues such as lymphoid organs, pancreas, intestine and skin. During embryogenesis, Sox4 regulates the survival of mesenchymal and neural progenitors, lymphocyte and myeloid differentiation, and pancreatic, bone and cardiac development. Aberrantly increased Sox4 expression is linked to malignant transformation and metastasis in several types of human cancer. To study the role of Sox4 in the adult organism, we first generated mice with reduced whole-body Sox4 expression. These mice display a plethora of age-related degenerative disorders and reduced spontaneous cancer incidence, indicating a role for this protein in maintaining adult tissue homeostasis and in tumor growth. To specifically address a role for Sox4 in adult stem cells, we conditionally deleted Sox4 (Sox4cKO) in stratified epithelia. Sox4cKO mice show increased skin stem cell quiescence and DNA damage accumulation, accompanied by resistance to chemical carcinogenesis. These phenotypes correlate with downregulation of cell cycle, DNA repair and skin stem cell genes in the absence of Sox4. Altogether, these findings highlight the importance of Sox4 in adult tissue homeostasis and cancer. Sox4 WT and cKO (conditional KO in skin) skin was collected for microarray hybridization, to study the contribution of Sox4 to skin homeostasis in basal conditions (Telogen)
2015-05-20 | E-GEOD-58154 | biostudies-arrayexpress
Project description:Sox4 is a transcription factor expressed during embryonic development and some adult tissues such as lymphoid organs, pancreas, intestine and skin. During embryogenesis, Sox4 regulates the survival of mesenchymal and neural progenitors, lymphocyte and myeloid differentiation, and pancreatic, bone and cardiac development. Aberrantly increased Sox4 expression is linked to malignant transformation and metastasis in several types of human cancer. To study the role of Sox4 in the adult organism, we first generated mice with reduced whole-body Sox4 expression. These mice display a plethora of age-related degenerative disorders and reduced spontaneous cancer incidence, indicating a role for this protein in maintaining adult tissue homeostasis and in tumor growth. To specifically address a role for Sox4 in adult stem cells, we conditionally deleted Sox4 (Sox4cKO) in stratified epithelia. Sox4cKO mice show increased skin stem cell quiescence and DNA damage accumulation, accompanied by resistance to chemical carcinogenesis. These phenotypes correlate with downregulation of cell cycle, DNA repair and skin stem cell genes in the absence of Sox4. Altogether, these findings highlight the importance of Sox4 in adult tissue homeostasis and cancer. Sox4 WT and cKO (conditional KO in skin) were plucked and skin was collected for microarray hibridization, to study the contribution of Sox4 to hair regeneration and hair follicle stem cell activation
2015-05-20 | E-GEOD-58153 | biostudies-arrayexpress
Project description:The neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL). We have recently demonstrated SOX11 tumorigenic potential in vivo by showing a significant reduction on tumor growth of SOX11-knockdown MCL cells in xenograft experiments, confirming the clinical observations that SOX11 may play an important role in the aggressive behavior of MCL (Vegliante et al., 2013). However, the specific mechanisms regulated by SOX11 that promote the oncogenic and rapid tumor growth of aggressive MCL still remain to be elucidated. To further characterize the potential oncogenic mechanisms regulated by SOX11 in MCL, we have analyzed the GEP derived from the xenograft SOX11-positive and knockdown xenograft derived tumors. Differential gene expression between SOX11-positive Z138 and SOX11-negative Z138 MCL cell lines xenotransplanted in SCID mices derived tumors.
2014-11-04 | GSE52892 | GEO
Project description:SOX11 and SOX4 drive the reactivation of an embryonic gene program during wound repair
| PRJNA494434 | ENA