Laminin binding/non-binding germ cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE829 | GEO | 2004/03/16
SECONDARY ACCESSION(S): PRJNA87827
REPOSITORIES: GEO
Similar Datasets
Project description:Comparison of laminin binding and laminin non-binding germ cells.
2007-12-19 | E-GEOD-829 | biostudies-arrayexpress
Project description:Laminin (merosin) deficient muscular dystrophy in dy/dy mouse diaphragm muscle, 8 weeks old Keywords: muscle, muscular dystrophy, laminin, merosin, diaphragm, mouse
2006-03-16 | GSE3252 | GEO
Project description:Mutations in the gene encoding laminin a2 chain cause congenital muscular dystrophy, MDC1A. In skeletal muscle, laminin a2 chain binds at least two receptor complexes; the dystrophin-glycoprotein complex and integrin a7b1. To gain insight into the molecular mechanisms underlying this disorder, we performed gene expression profiling of laminin a2 chain deficient mouse limb muscle. One of the down-regulated genes encodes a protein called calcium and integrin binding protein 2 (Cib2) whose expression and function is unknown. However, the closely related Cib1 has been reported to bind integrin aIIb and may be involved in outside-in-signaling in platelets. Since Cib2 might be a novel integrin a7b1 binding protein in muscle, we have studied Cib2 expression in the developing and adult mouse. Cib2 mRNA is mainly expressed in the developing central nervous system and in developing and adult skeletal muscle. In skeletal muscle Cib2 colocalizes with integrin a7B subunit at the sarcolemma and at the neuromuscular- and myotendinous junctions. Finally, we demonstrate that Cib2 is a calcium binding protein that interacts with integrin a7Bb1D. Thus, our data suggest a role for Cib2 as a cytoplasmic effector of integrin a7Bb1D signaling in skeletal muscle Keywords: disese state analysis
2008-07-10 | GSE12049 | GEO
Project description:Integrin dimers a3/b1, a6/b1 and a6/b4 are the receptors of mammary epithelial cells for Laminin, major component of the mammary basement membrane. Antibodies against a6 and a3 integrin chains serve to isolate stem cell enriched populations from mammary epithelium, however, role of integrin dimers comprising these chains in the control of mammary stem cell activity are not known. To investigate the role of Laminin-binding integrins in the control of mammary stem cell function, a3 and a6 chains were deleted from mammary basal cells in vitro using Cre-recombinase carrying adenovirus. We found that deletion of single integrin chain (either a3, or a6) did not significantly affect stem cell potential as evaluated by transplantation and mammosphere assays, whereas basal cells depleted of both a3 and a6 integrin chains (a3a6KO) presented severely diminished stem cell activity. In this study the transcriptional profiles of a3a6KO were analysed and compared to those of control cells.
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Project description:E2F in vivo binding specificity: comparison of consensus vs. non-consensus binding sites
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Project description:Integrin dimers α3/β1, α6/β1 and α6/β4 are the mammary epithelial cell receptors for laminins, which are major components of the basement membrane, a specialized extracellular matrix surrounding the mammary epithelium. The roles of specific basement membrane components and their integrin receptors in the regulation of functional gland development have not been analyzed in detail. To investigate the functions of laminin-binding integrins, we obtained mutant mice with mammary luminal cell-specific deficiencies of the α3 and α6 integrin chains generated by the Cre-Lox approach. During pregnancy, mutant mice displayed low levels of luminal progenitor activity and retarded lobulo-alveolar development, whereas their mammary glands seemed to be functional at the onset of lactation. Myoepithelial cell morphology was markedly altered in mutant glands, suggesting cellular compensation mechanisms involving cytoskeleton reorganization. However, lactation was not sustained in mutant mice, and the glands underwent precocious involution. Inactivation of the p53 gene rescued the growth defects but did not restore lactogenesis in mutant mice. This study reveals an essential role for laminin-binding integrins in functional mammary gland development.
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Project description:Comparison of miRNA expression profiles in malignant germ cell tumors compared to non-malignant control group. Use of bioinformatic algorithm Sylamer to interrogate mRNA expression profiles from malignant germ cell tumors for enrichment or depletion of binding sites for differentially expressed miRNAs. Use of Gene Ontology (GO) analysis to demonstrate functional significance of differentially expressed miRNAs in malignant germ cell tumors.
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Project description:Deciphering the mammary stem cell niche: a role for laminin-binding integrins
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Project description:Mutations in the gene encoding laminin a2 chain cause congenital muscular dystrophy, MDC1A. In skeletal muscle, laminin a2 chain binds at least two receptor complexes; the dystrophin-glycoprotein complex and integrin a7b1. To gain insight into the molecular mechanisms underlying this disorder, we performed gene expression profiling of laminin a2 chain deficient mouse limb muscle. One of the down-regulated genes encodes a protein called calcium and integrin binding protein 2 (Cib2) whose expression and function is unknown. However, the closely related Cib1 has been reported to bind integrin aIIb and may be involved in outside-in-signaling in platelets. Since Cib2 might be a novel integrin a7b1 binding protein in muscle, we have studied Cib2 expression in the developing and adult mouse. Cib2 mRNA is mainly expressed in the developing central nervous system and in developing and adult skeletal muscle. In skeletal muscle Cib2 colocalizes with integrin a7B subunit at the sarcolemma and at the neuromuscular- and myotendinous junctions. Finally, we demonstrate that Cib2 is a calcium binding protein that interacts with integrin a7Bb1D. Thus, our data suggest a role for Cib2 as a cytoplasmic effector of integrin a7Bb1D signaling in skeletal muscle Experiment Overall Design: Skeletal muscle (all hind limb skeletal muscle) from 4-weeks old laminin alpha 2 chain deficient mice and 4-weeks old wild type mice were isolated individually and RNA were extracted and hybridized on Affiymetrix microarrys. Three biological replicates from each group were analyzed.
2008-10-21 | E-GEOD-12049 | biostudies-arrayexpress