Annexin A11 in disease

Ubiquitously expressed in many cell types, annexin A11 (Anxa11) is a member of the multigene family of Ca2+-regulated phospholipid-dependent and membrane-binding annexin proteins. Studies have shown that Anxa11 plays an important role in cell division, Ca2+ signaling, vesicle trafficking and apoptos...

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Published inClinica chimica acta Vol. 431; pp. 164 - 168
Main Authors Wang, Jiasheng, Guo, Chunmei, Liu, Shuqing, Qi, Houbao, Yin, Yuling, Liang, Rui, Sun, Ming-Zhong, Greenaway, Frederick T.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 20.04.2014
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Summary:Ubiquitously expressed in many cell types, annexin A11 (Anxa11) is a member of the multigene family of Ca2+-regulated phospholipid-dependent and membrane-binding annexin proteins. Studies have shown that Anxa11 plays an important role in cell division, Ca2+ signaling, vesicle trafficking and apoptosis. The deregulation and mutation of Anxa11 are involved in systemic autoimmune diseases, sarcoidosis and the development, chemoresistance and recurrence of cancers. Malfunction of Anxa11 may lead to or enhance the metastasis, invasion and drug resistance of cancers through the platelet-derived growth factor receptor (PDGFR) pathway and/or the mitogen-activated protein kinase (MAPK)/p53 pathway. In a variety of diseases, Anxa11 is most commonly reported to function through interactions with apoptosis-linked gene-2 protein (ALG-2) and/or calcyclin (S100A6). Although it has been little studied, Anxa11 is a promising biomarker for the diagnosis, treatment and prognosis of certain diseases. In this review, the associations of Anxa11 with Ca2+-regulated exocytosis, cytokinesis, sex differentiation, autoimmune diseases, thrombolysis and cancers are summarized and interpreted. •Anxa11 is critical for exocytosis, cytokinesis and sex differentiation.•Anxa11 is a potential indicator for autoimmune diseases and benefits thrombolysis.•Anxa11 is deregulated in a variety of cancers.•Anxa11 contributes to progression and development of cancers.
Bibliography:ObjectType-Article-2
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ISSN:0009-8981
1873-3492
DOI:10.1016/j.cca.2014.01.031