The TAGLN gene and its putative association with human ageing

Cell Senescence Entries for TAGLN

Cell Types: Liver cancer
Cell Lines: Hep G2
Cancer Cell?: Yes
Method: Knockdown, Overexpression
Type of senescence: Stress-induced
Senescence Effect: Induces
Primary Reference: Kim et al. (2010) SM22α-induced activation of p16INK4a/retinoblastoma pathway promotes cellular senescence caused by a subclinical dose of γ-radiation and doxorubicin in HepG2 cells. Biochem Biophys Res Commun 400(1)100-5 (PubMed)

HGNC symbol: TAGLN
Aliases: DKFZp686P11128; SM22; SMCC; TAGLN1; WS3-10
Common name: transgelin
Entrez Id: 6876
Description: 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].

Gene Ontology

Process:

GO:30855; epithelial cell differentiation
GO:7517; muscle organ development

Cellular component:

GO:5737; cytoplasm
GO:5856; cytoskeleton

Function:

GO:3779; actin binding
GO:51015; actin filament binding
GO:5515; protein binding

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