| cell adhesion molecule 1 | OKDB#: 4632 |
| Symbols: | CADM1 | Species: | human | ||
| Synonyms: | BL2, ST17, IGSF4, NECL2, RA175, TSLC1, IGSF4A, Necl-2, SYNCAM, sgIGSF, sTSLC-1, synCAM1,BL2, ST17, IGSF4, NECL2, RA175, TSLC1, IGSF4A, Necl-2, SYNCAM, sgIGSF, sTSLC-1, synCAM1, | Locus: | 11q23.2 in Homo sapiens |
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| General Comment | |||||
| General function | Cell adhesion molecule | ||||
| Comment | |||||
| Cellular localization | Plasma membrane | ||||
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| Ovarian function | |||||
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| Expression regulated by | |||||
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| Ovarian localization | Granulosa | ||||
| Comment | Characterization and Significance of Adhesion and Junction-Related Proteins in Mouse Ovarian Follicles. Mora JM et al. In the ovary, initiation of follicle growth is marked by cuboidalization of flattened granulosa cells (GCs). The regulation and cell biology of this shape change remains poorly understood. We propose that characterization of intercellular junctions and associated proteins is key to identifying as yet unknown regulators of this important transition. As GCs are conventionally described as epithelial, this study used mouse ovaries and isolated follicles to investigate epithelial junctional complexes (tight junctions [TJ], adherens junctions [AJ] and desmosomes) and associated molecules, as well as classic epithelial markers by quantitative PCR and immunofluorescence. These junctions were further characterized using ultrastructural, calcium-depletion and biotin tracer studies. Junctions observed by transmission electron microscopy between GCs and between GCs and the oocyte were identified as AJs by expression of N-cadherin and nectin 2, and by lack of TJ and desmosome-associated proteins. Follicles were also permeable to biotin confirming a lack of functional TJs. Surprisingly, GCs lacked all epithelial markers analysed, including E-cadherin, cytokeratin 8, and zonula occludens (ZO)-1alpha+. Furthermore, vimentin was expressed by GCs suggesting a more mesenchymal phenotype. In calcium-free conditions, small follicles maintained oocyte-GC contact confirming the importance of calcium-independent nectin at this stage. However, in primary and multilayered follicles, lack of calcium resulted in loss of contact between GCs and oocyte, showing that nectin alone cannot maintain attachment between these two cell types. Lack of classic markers suggests that GCs are not epithelial. Identification of AJs during GC cuboidalization highlights the importance of AJs in regulating initiation of follicle growth. | ||||
| Follicle stages | Corpus luteum | ||||
| Comment | Human chorionic gonadotropin controls luteal vascular permeability via vascular endothelial growth factor by down-regulation of a cascade of adhesion proteins. Herr D et al. OBJECTIVE: To study the functional interactions of junctional proteins acting as regulators of vascular permeability in the human corpus luteum. We investigated the role of vascular endothelial (VE)-cadherin, nectin 2, and claudin 5 as controllers of vascular endothelial cell permeability. DESIGN: Performing immunohistochemical dual staining, we colocalized the above-mentioned proteins in the human corpus luteum. SETTING: Not applicable. PATIENT(S): Not applicable. INTERVENTION(S): Not applicable. MAIN OUTCOME MEASURE(S): Using a granulosa-endothelial coculture system, we revealed that hCG-treatment down-regulates VE-cadherin, nectin 2, and claudin 5 in endothelial cells via vascular endothelial growth factor (VEGFA). RESULT(S): Furthermore, the interaction of VE-cadherin, nectin 2, and claudin 5 was investigated by silencing these proteins that perform siRNA knockdown. Interestingly, knockdown of VE-cadherin and claudin 5 induced a decrease of the respective other protein. This down-regulation was associated with changed rates of vascular permeability: hCG induced a VEGFA-dependent down-regulation of VE-cadherin, nectin 2, and claudin 5, which increased the endothelial permeability in the coculture system. Furthermore, knockdown of VE-cadherin, nectin-2, and claudin 5 also resulted in a consecutive increase of endothelial permeability for each different protein. CONCLUSION(S): These results demonstrate for the first time that VE-cadherin, nectin 2, and claudin 5 are involved in the regulation of vascular permeability in a mutually interacting manner, which indicates their prominent role for the functionality of the human corpus luteum. | ||||
| Phenotypes | |||||
| Mutations | 0 mutations | ||||
| Genomic Region | show genomic region | ||||
| Phenotypes and GWAS | show phenotypes and GWAS | ||||
| Links |
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| created: | Feb. 20, 2012, 5:14 p.m. | by: |
hsueh email:
home page: |
| last update: | April 5, 2013, 3:40 p.m. | by: | hsueh email: |
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