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Gene Symbol |
TAGLN |
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Aliases |
SM22, SM22-alpha, SMCC, TAGLN1, WS3-10 |
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Entrez Gene ID |
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Gene Name |
Transgelin |
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Chromosomal Location |
11q23.3 |
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HGNC ID |
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Summary |
This gene encodes a shape change and transformation sensitive actin-binding protein which belongs to the calponin family. It is ubiquitously expressed in vascular and visceral smooth muscle, and is an early marker of smooth muscle differentiation. The encoded protein is thought to be involved in calcium-independent smooth muscle contraction. It acts as a tumor suppressor, and the loss of its expression is an early event in cell transformation and the development of some tumors, coinciding with cellular plasticity. The encoded protein has a domain architecture consisting of an N-terminal calponin homology (CH) domain and a C-terminal calponin-like (CLIK) domain. Mice with a knockout of the orthologous gene are viable and fertile but their vascular smooth muscle cells exhibit alterations in the distribution of the actin filament and changes in cytoskeletal organization. [provided by RefSeq, Aug 2017]
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e!Ensembl
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Protein Information |
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Protein Name |
Transgelin, 22 kDa actin-binding protein, epididymis secretory sperm binding protein, smooth muscle protein 22-alpha, transgelin variant 2 |
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Function |
Actin cross-linking/gelling protein (By similarity). Involved in calcium interactions and contractile properties of the cell that may contribute to replicative senescence. |
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UniProt |
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Interactions |
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STRING |
MINT |
IntAct |
ENSP00000325527 |
P35555 |
P35555 |
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View interactions
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Associated Diseases
Disease group | Disease Name | References |
Endocrine System Diseases |
PCOS |
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Neoplasms |
Colonic Neoplasms |
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Breast Cancer |
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Esophagus Neoplasm |
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Nutritional and Metabolic Diseases |
Lipoidosis |
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Reproductive disorders |
Endometrioma |
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Endometriosis |
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References |
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Galazis Nicolas, Pang Yik-Lam, Galazi Myria, Haoula Zeina, Layfield Robert, Atiomo William |
Nottingham Medical School, University of Nottingham, Queen's Medical Centre Campus Nottingham University Hospital, Nottingham, UK. ngalazis@gmail.com |
Gynecol Endocrinol. 2013 Jul;29(7):638-44. doi: 10.3109/09513590.2013.777416. |
Abstract
There is a need for research studies into the molecular mechanisms underpinning the link between polycystic ovary syndrome (PCOS) and endometrial cancer (EC) to facilitate screening and to encourage the development of novel strategies to prevent disease progression. The objective of this review was to identify proteomic biomarkers of EC risk in women with PCOS. All eligible published studies on proteomic biomarkers for EC identified through the literature were evaluated. Proteomic biomarkers for EC were then integrated with an updated previously published database of all proteomic biomarkers identified so far in PCOS women. Nine protein biomarkers were similarly either under or over expressed in women with EC and PCOS in various tissues. These include transgelin, pyruvate kinase M1/M2, gelsolin-like capping protein (macrophage capping protein), glutathione S-transferase P, leucine aminopeptidase (cytosol aminopeptidase), peptidyl-prolyl cis-transisomerase, cyclophilin A, complement component C4A and manganese-superoxide dismutase. If validated, these biomarkers may provide a useful framework on which the knowledge base in this area could be developed and will facilitate future mathematical modelling to enhance screening and prevention of EC in women with PCOS who have been shown to be at increased risk. |
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| © 2019, Biomedical Informatics Centre, NIRRH |
National Institute for Research in Reproductive Health, Jehangir Merwanji Street, Parel, Mumbai-400 012
Tel: 91-22-24192104, Fax No: 91-22-24139412
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