Literature DB >> 17526423

Flightless I: an actin-remodelling protein and an important negative regulator of wound repair.

Z Kopecki1, A J Cowin.   

Abstract

Flightless I (FliI) is a member of the gelsolin family of actin-remodelling proteins, and has been identified as having two functional protein family domains: a leucine rich repeat (LRR) domain and a gelsolin-like domain. This unique structure allows FliI to act as an actin-remodelling protein as well as a nuclear receptor co-activator with ability to interact with various other proteins important in cellular signaling. The actin cytoskeleton is an integral component of all cells and the effect of FliI protein on actin remodelling is a vital part of cellular motility, contraction and adhesion. The product of the FliI gene is expected to provide a vital link between the molecules of yet unidentified signal transduction pathways and the actin cytoskeleton. Exact signaling pathways and mechanisms underpinning FliI effects in wound healing are yet to be fully identified however strong research evidence clearly identifies this molecule as a possible new therapeutic target whose manipulation may greatly improve wound healing and could lead to potential innovative medical applications.

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Year:  2007        PMID: 17526423     DOI: 10.1016/j.biocel.2007.04.011

Source DB:  PubMed          Journal:  Int J Biochem Cell Biol        ISSN: 1357-2725            Impact factor:   5.085


  25 in total

1.  Amotl2 interacts with LL5β, localizes to podosomes and regulates postsynaptic differentiation in muscle.

Authors:  Tomasz J Proszynski; Joshua R Sanes
Journal:  J Cell Sci       Date:  2013-03-22       Impact factor: 5.285

2.  The signaling adaptor BCAP inhibits NLRP3 and NLRC4 inflammasome activation in macrophages through interactions with Flightless-1.

Authors:  Samuel J Carpentier; Minjian Ni; Jeffrey M Duggan; Richard G James; Brad T Cookson; Jessica A Hamerman
Journal:  Sci Signal       Date:  2019-05-14       Impact factor: 8.192

3.  Decreased expression of Flightless I, a gelsolin family member and developmental regulator, in early-gestation fetal wounds improves healing.

Authors:  Cheng-Hung Lin; James M Waters; Barry C Powell; Ruth M Arkell; Allison J Cowin
Journal:  Mamm Genome       Date:  2011-03-13       Impact factor: 2.957

4.  Flightless-I homolog regulates glucocorticoid receptor-mediated transcription via direct interaction of the leucine-rich repeat domain.

Authors:  Hong Lan Jin; Liu Yang; Kwang Won Jeong
Journal:  Mol Biol Rep       Date:  2017-04-28       Impact factor: 2.316

5.  Response of Leucine-Rich Repeat Domain-Containing Protein in Haemaphysalis longicornis to Babesia microti Infection and Its Ligand Identification.

Authors:  Jialing Yao; Zhengmao Xu; Zeyu Sun; Keke Zhou; Jinmiao Lu; Rongsheng Mi; Yan Huang; Xiangan Han; Keyi Ren; Zhaoguo Chen; Haiyan Gong
Journal:  Infect Immun       Date:  2021-04-16       Impact factor: 3.441

6.  Flii control: balancing migration and adhesion.

Authors:  Kristina Kligys; Jonathan C R Jones
Journal:  J Invest Dermatol       Date:  2009-08       Impact factor: 8.551

Review 7.  Nuclear actin and actin-binding proteins in the regulation of transcription and gene expression.

Authors:  Bin Zheng; Mei Han; Michel Bernier; Jin-kun Wen
Journal:  FEBS J       Date:  2009-05       Impact factor: 5.542

8.  Flightless-I is a potential biomarker for the early detection of alcoholic liver disease.

Authors:  Jaime Arellanes-Robledo; Joseph Ibrahim; Karina Reyes-Gordillo; Ruchi Shah; Leslie Leckey; M Raj Lakshman
Journal:  Biochem Pharmacol       Date:  2020-11-07       Impact factor: 5.858

Review 9.  A Review of Acquired Autoimmune Blistering Diseases in Inherited Epidermolysis Bullosa: Implications for the Future of Gene Therapy.

Authors:  Payal M Patel; Virginia A Jones; Christy T Behnam; Giovanni Di Zenzo; Kyle T Amber
Journal:  Antibodies (Basel)       Date:  2021-05-17

10.  Flightless I is a catabolic factor of chondrocytes that promotes hypertrophy and cartilage degeneration in osteoarthritis.

Authors:  Taku Ebata; Mohamad Alaa Terkawi; Masanari Hamasaki; Gen Matsumae; Tomohiro Onodera; Mahmoud Khamis Aly; Shunichi Yokota; Hend Alhasan; Tomohiro Shimizu; Daisuke Takahashi; Kentaro Homan; Ken Kadoya; Norimasa Iwasaki
Journal:  iScience       Date:  2021-05-24
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