Ignet
Search (e.g., vaccine, IFNG): Help
About
Home
Introduction
Statistics
Programs
Dignet
Gene
GenePair
BioSummarAI
Help & Docs
Documents
Help
FAQs
Links
Acknowledge
Disclaimer
Contact Us
UM Logo

UMMS Logo

UMMS Logo

Gene Information

Gene symbol: ACTR2

Gene name: ARP2 actin-related protein 2 homolog (yeast)

HGNC ID: 169

Synonyms: ARP2

Related Genes

# Gene Symbol Number of hits
1 ARFRP1 1 hits
2 AVIL 1 hits
3 CDC42 1 hits
4 CTTN 1 hits
5 EGF 1 hits
6 NTRK3 1 hits
7 PLCE1 1 hits
8 RAC1 1 hits
9 SYNPO 1 hits
10 WAS 1 hits
11 WASF1 1 hits

Related Sentences

# PMID Sentence
1 11553524 CD2AP and p130Cas localize to different F-actin structures in podocytes.
2 11553524 Mice lacking the 80-kDa CD2-associated protein (CD2AP) develop progressive renal failure that starts soon after birth with proteinuria and foot process effacement by unknown mechanisms.
3 11553524 CD2AP has been identified and cloned independently by virtue of its interaction with the T cell protein CD2 and with the docking protein p130Cas.
4 11553524 In the present study we examined the localization of CD2AP and p130Cas in the mouse glomerulus and in cultured podocytes.
5 11553524 In glomeruli, CD2AP and p130Cas immunofluorescence were observed in podocytes, where they colocalized with F-actin in foot processes.
6 11553524 In cultured podocytes, p130Cas was enriched at sites of focal adhesions, where it colocalized like vinculin with F-actin at stress fiber ends.
7 11553524 The spot-shaped F-actin structures were also stained by antibodies against the actin nucleation Arp2/3 complex and cortactin, both contributing to dynamic actin assembly.
8 11553524 Moreover, CD2AP spots in cultured podocytes were in close spatial association with actinin-4, but not actinin-1.
9 11553524 Our results suggest that CD2AP and p130Cas, which both colocalize with F-actin in podocytes in situ, possess different functions.
10 11553524 Whereas p130Cas is found in focal adhesions, CD2AP seems to be involved in the regulation of highly dynamic F-actin structures in podocyte foot processes.
11 29058690 Advillin acts upstream of phospholipase C ϵ1 in steroid-resistant nephrotic syndrome.
12 29058690 Additionally, AVIL colocalized and interacted with the phospholipase enzyme PLCE1 and with the ARP2/3 actin-modulating complex.
13 29058690 Knockdown of AVIL in human podocytes reduced actin stress fibers at the cell periphery, prevented recruitment of PLCE1 to the ARP3-rich lamellipodia, blocked EGF-induced generation of diacylglycerol (DAG) by PLCE1, and attenuated the podocyte migration rate (PMR).
14 29058690 The PMR was increased by overexpression of WT Avil or PLCE1, or by EGF stimulation; however, this increased PMR was ameliorated by inhibition of the ARP2/3 complex, indicating that ARP-dependent lamellipodia formation occurs downstream of AVIL and PLCE1 function.
15 29058690 Together, these results delineate a comprehensive pathogenic axis of SRNS that integrates loss of AVIL function with alterations in the action of PLCE1, an established SRNS protein.
16 29058690 Advillin acts upstream of phospholipase C ϵ1 in steroid-resistant nephrotic syndrome.
17 29058690 Additionally, AVIL colocalized and interacted with the phospholipase enzyme PLCE1 and with the ARP2/3 actin-modulating complex.
18 29058690 Knockdown of AVIL in human podocytes reduced actin stress fibers at the cell periphery, prevented recruitment of PLCE1 to the ARP3-rich lamellipodia, blocked EGF-induced generation of diacylglycerol (DAG) by PLCE1, and attenuated the podocyte migration rate (PMR).
19 29058690 The PMR was increased by overexpression of WT Avil or PLCE1, or by EGF stimulation; however, this increased PMR was ameliorated by inhibition of the ARP2/3 complex, indicating that ARP-dependent lamellipodia formation occurs downstream of AVIL and PLCE1 function.
20 29058690 Together, these results delineate a comprehensive pathogenic axis of SRNS that integrates loss of AVIL function with alterations in the action of PLCE1, an established SRNS protein.
21 29162704 Tropomyosin-related kinase C (TrkC) enhances podocyte migration by ERK-mediated WAVE2 activation.
22 29162704 Activation of endogenous TrkC by its ligand neurotrophin-3 resulted in increased podocyte migration-a surrogate of podocyte actin dynamics in vivo.
23 29162704 Employing a mutagenesis approach, we found that the Src homologous and collagen-like (Shc) binding site Tyr516 within the TrkC cytoplasmic domain was necessary for TrkC-induced migration of podocytes.
24 29162704 TrkC activation led to a mobility shift of Wiskott-Aldrich syndrome family verprolin-homologous protein (WAVE)-2 which is known to orchestrate Arp2/3 activation and actin polymerization.
25 29162704 Chemical inactivation of Erk or mutagenesis of 2 of 4 known Erk target sites within WAVE2, Thr346 and Ser351, abolished the TrkC-induced WAVE2 mobility shift.
26 29162704 Knockdown of WAVE2 by shRNA abolished TrkC-induced podocyte migration.
27 29162704 In summary, TrkC signals to the podocyte actin cytoskeleton to induce migration by phosphorylating WAVE2 Erk dependently.
28 33308016 The present study explored whether Add3 contributes to the modulation of podocyte structure and function using FHH and FHH.
29 33308016 We found that F-actin nets, which are typically localized in the lamellipodia, replaced unbranched stress fibers in conditionally immortalized mouse podocytes transfected with Add3 Dicer-substrate short interfering RNA (DsiRNA) and primary podocytes isolated from FHH rats.
30 33308016 There were increased F/G-actin ratios and expression of the Arp2/3 complexes throughout FHH podocytes in association with reduced synaptopodin and RhoA but enhanced Rac1 and CDC42 expression in the renal cortex, glomeruli, and podocytes of FHH rats.