Actin Depolymerizing Factors (Cofilins)

A family of low MOLECULAR WEIGHT actin-binding proteins found throughout eukaryotes. They remodel the actin CYTOSKELETON by severing ACTIN FILAMENTS and increasing the rate of monomer dissociation.

Also Known As:

Cofilins; ADF Proteins (Actin Depolymerizing Factors); Actin Depolymerizing Proteins; Cofilin Proteins; Depolymerizing Factors, Actin; Depolymerizing Protein, Actin; Depolymerizing Proteins, Actin; Protein, Actin Depolymerizing; Actin Depolymerizing Protein; Cofilin

Networked: 508 relevant articles (7 outcomes, 66 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Bamburg, James R: 17 articles (10/2021 - 12/2005)
2.	Condeelis, John: 11 articles (12/2014 - 08/2004)
3.	Minamide, Laurie S: 8 articles (10/2021 - 12/2005)
4.	Shah, Zahoor A: 7 articles (01/2022 - 02/2016)
5.	Cho, Min Chul: 7 articles (12/2021 - 05/2015)
6.	Kim, Soo Woong: 7 articles (12/2021 - 05/2015)
7.	Wu, Yuntao: 7 articles (01/2021 - 10/2008)
8.	Alhadidi, Qasim: 6 articles (01/2022 - 02/2016)
9.	Gao, Ning: 6 articles (01/2022 - 07/2013)
10.	Shaw, Alisa E: 6 articles (01/2018 - 05/2012)

Related Diseases

1.	Cognitive Dysfunction 11/17/2023 - "The activation of extrinsically disordered LIMK1 in vivo improved memory encoding and slowed cognitive decline in aged mice exhibiting reduced cofilin phosphorylation. " 03/01/2023 - "Our study sheds new light on the role of PirB as an important mediator in modulating the dysfunction of synaptic plasticity and cognitive function via the RhoA/ROCK2/LIMK1/cofilin signalling pathway, which indicated that hippocampal PirB is a promising therapeutic target for counteracting cognitive impairment after CSR. " 12/01/2023 - "In conclusion, our findings suggest that diabetes leads to cognitive impairment, activation of the TRPM7/CaN/cofilin pathway, actin dynamics imbalance, and destruction of hippocampal neuronal cells and synapses. " 03/01/2023 - "PirB knockdown reverses cognitive impairment and synaptic plasticity disorders caused by CSR through the RhoA/ROCK2/LIMK1/cofilin signalling pathway." 03/01/2023 - "PirB knockdown alleviated synaptic deficits and cognitive impairment after CSR by inhibiting the RhoA/ROCK2/LIMK1/cofilin signalling pathway. "
2.	Glioma (Gliomas) 09/26/2017 - "miR-29a/b/c overexpressions suppressed glioma cell migration and invasion through targeting CDC42 and subsequently decreasing phosphorylated PAK1/2/3, LIMK1/2 and cofilin, the pivotal downstream effectors of CDC42. " 06/01/2017 - "Our data indicated that miR-451 relays environmental signals by upregulating the activity of AMPK signaling, thereby modulating the activation of mTOR and Rac1/cofilin which, in turn, play key roles in glioma cell proliferation and migration, respectively. " 06/01/2016 - "Nogo-A may inhibit the migration and invasion of human malignant glioma cells via the downregulation of RhoA-cofilin signaling. " 04/01/2016 - "In conclusion, SEPT7 is involved in glioma cell migration with the assistance of cofilin phospho‑mediated cytoskeleton locomotion." 04/01/2016 - "The data revealed that the F‑actin/G‑actin ratio and cofilin were reduced, and p‑cofilin increased conversely in cells with SEPT7 overexpression, indicating that SEPT7 reduced glioma cell migration by promoting cofilin phosphorylation and depolymerizing actin. "
3.	Ischemia 01/01/2018 - "Interventions that limit cofilin-actin rod formation may help to preserve integrity of neuronal processes in permanent ischemia." 03/01/2016 - "The expression profile studies demonstrated a decrease in phosphocofilin levels in all models of ischemia, implying stress-induced cofilin activation. " 03/01/2016 - "In the present study, we have hypothesized the possible involvement of cofilin in ischemia. " 01/01/2023 - "Herein, we hypothesized that RPC would mitigate hippocampal synaptic dysfunction and pathological cofilin hyperactivation in an ex vivo model of ischemia. " 01/01/2020 - "Immunostaining and TdT-mediated dUTP Nick-End Labeling (TUNEL) apoptosis staining were collaboratively used to examine cofilin rod formation and cell apoptosis in response to ischemia at different time points (2 h, 8 h, 24 h and 7 d). "
4.	Amyloid Plaque 01/01/2014 - "Instead, data suggest the involvement of microglia in the clearance of cofilin rods/aggregates and/or in their synthesis in and around amyloid plaques and surrounding neuropil. " 01/01/2020 - "However, several cellular biological signatures of AD have been identified such as synaptic dysfunction, β-amyloid plaques, hyperphosphorylated tau, cofilin-actin rods, and Hirano bodies which are related to the actin cytoskeleton. " 01/01/2014 - "Taken together these data suggest that RanBP9 overexpression down-regulates cofilin, causes early synaptic deficits and impaired learning, and accelerates accumulation of amyloid plaques in the mouse brain." 01/01/2014 - "RanBP9 overexpression down-regulates phospho-cofilin, causes early synaptic deficits and impaired learning, and accelerates accumulation of amyloid plaques in the mouse brain." 01/01/2019 - "In addition to amyloid plaques and neurofibrillary tangles, AD brains contain Hirano bodies, which are rod-like structures mostly composed of actin and the actin-binding protein, cofilin. "
5.	Wounds and Injuries (Trauma) 11/01/2011 - "Cofilin siRNA greatly attenuated the ability of VSMC migration into the "wound," and platelet-derived growth factor (PDGF)-induced migration was virtually eliminated versus a 3.5-fold increase in nontreated VSMCs, establishing a critical role for cofilin in VSMC migration. " 11/01/2011 - "Scratch wound and modified Boyden chamber assays were used to assess VSMC migration following downregulation of the expression of cofilin and each SSH phosphatase isoform (SSH1, SSH2, and SSH3) by small interfering RNA (siRNA), respectively. " 10/01/2017 - "Silencing Zonula occludens 2 (ZO-2), a tight junctions (TJ) scaffold protein, in epithelial cells (MDCK ZO-2 KD) triggers: 1) Decreased cell to substratum attachment, accompanied by reduced expression of claudin-7 and integrin β1, and increased vinculin recruitment to focal adhesions and stress fibers formation; 2) Lowered cell-cell aggregation and appearance of wider intercellular spaces; 3) Increased RhoA/ROCK activity, mediated by GEF-HI recruitment to cell borders by cingulin; 4) Increased Cdc42 activity, mitotic spindle disorientation and the appearance of cysts with multiple lumens; 5) Increased Rac and cofilin activity, multiple lamellipodia formation and random cell migration but increased wound closure; 6) Diminished cingulin phosphorylation and disappearance of planar network of microtubules at the TJ region; and 7) Increased transepithelial electrical resistance at steady state, coupled to an increased expression of ZO-1 and claudin-4 and a decreased expression of claudin-2 and paracingulin. " 01/01/2022 - "Other assays include nitric oxide (NO) by Griess reagent, cofilin inhibition by F-actin depolymerization, migration by scratch wound assay, tumor necrosis factor (TNF-α) by enzyme-linked immunosorbent assay (ELISA), protease-activated receptor-1 (PAR-1) by immunocytochemistry and Western blotting (WB), and protein expression levels of several proteins by WB. "

Related Drugs and Biologics

1.	Small Interfering RNA (siRNA)
2.	Platelet-Derived Growth Factor
3.	Huntingtin Protein
4.	Proteins (Proteins, Gene)
5.	Actins (F Actin)
6.	Destrin (Actin Depolymerizing Factor)
7.	Lim Kinases
8.	Phosphotransferases (Kinase)
9.	Profilins (Profilin)
10.	Actin-Related Protein 2-3 Complex (Arp2 3 Complex)

Related Therapies and Procedures

1.	Therapeutics
2.	Electroacupuncture
3.	Radiotherapy
4.	Moxibustion
5.	Drug Therapy (Chemotherapy)