Universität zu Köln

Wolff, Lisa ORCID: 0000-0002-7296-0479, Strathmann, Eike A., Mueller, Ilka, Maehlich, Daniela, Veltman, Charlotte, Niehoff, Anja and Wirth, Brunhilde ORCID: 0000-0003-4051-5191 (2021). Plastin 3 in health and disease: a matter of balance. Cell. Mol. Life Sci., 78 (13). S. 5275 - 5302. BASEL: SPRINGER BASEL AG. ISSN 1420-9071

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Abstract

For a long time, PLS3 (plastin 3, also known as T-plastin or fimbrin) has been considered a rather inconspicuous protein, involved in F-actin-binding and -bundling. However, in recent years, a plethora of discoveries have turned PLS3 into a highly interesting protein involved in many cellular processes, signaling pathways, and diseases. PLS3 is localized on the X-chromosome, but shows sex-specific, inter-individual and tissue-specific expression variability pointing towards skewed X-inactivation. PLS3 is expressed in all solid tissues but usually not in hematopoietic cells. When escaping X-inactivation, PLS3 triggers a plethora of different types of cancers. Elevated PLS3 levels are considered a prognostic biomarker for cancer and refractory response to therapies. When it is knocked out or mutated in humans and mice, it causes osteoporosis with bone fractures; it is the only protein involved in actin dynamics responsible for osteoporosis. Instead, when PLS3 is upregulated, it acts as a highly protective SMN-independent modifier in spinal muscular atrophy (SMA). Here, it seems to counteract reduced F-actin levels by restoring impaired endocytosis and disturbed calcium homeostasis caused by reduced SMN levels. In contrast, an upregulation of PLS3 on wild-type level might cause osteoarthritis. This emphasizes that the amount of PLS3 in our cells must be precisely balanced; both too much and too little can be detrimental. Actin-dynamics, regulated by PLS3 among others, are crucial in a lot of cellular processes including endocytosis, cell migration, axonal growth, neurotransmission, translation, and others. Also, PLS3 levels influence the infection with different bacteria, mycosis, and other pathogens.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Wolff, Lisa UNSPECIFIED orcid.org/0000-0002-7296-0479 UNSPECIFIED Strathmann, Eike A. UNSPECIFIED UNSPECIFIED UNSPECIFIED Mueller, Ilka UNSPECIFIED UNSPECIFIED UNSPECIFIED Maehlich, Daniela UNSPECIFIED UNSPECIFIED UNSPECIFIED Veltman, Charlotte UNSPECIFIED UNSPECIFIED UNSPECIFIED Niehoff, Anja UNSPECIFIED UNSPECIFIED UNSPECIFIED Wirth, Brunhilde UNSPECIFIED orcid.org/0000-0003-4051-5191 UNSPECIFIED
URN:	urn:nbn:de:hbz:38-576840
DOI:	10.1007/s00018-021-03843-5
Journal or Publication Title:	Cell. Mol. Life Sci.
Volume:	78
Number:	13
Page Range:	S. 5275 - 5302
Date:	2021
Publisher:	SPRINGER BASEL AG
Place of Publication:	BASEL
ISSN:	1420-9071
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language SPINAL MUSCULAR-ATROPHY; EPITHELIAL-MESENCHYMAL TRANSITION; EARLY-ONSET OSTEOPOROSIS; COLON-CANCER RECURRENCE; FILAMENT CROSS-LINKING; X-LINKED OSTEOPOROSIS; T-PLASTIN; GENE-EXPRESSION; OSTEOGENESIS IMPERFECTA; ABERRANT EXPRESSION Multiple languages Biochemistry & Molecular Biology; Cell Biology Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/57684