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Decreased ARL2 expression level was clinically correlated to the higher grades and poorer outcomes of glioma patients. ARL2 overexpression attenuated the proliferation, clone formation, migration, invasive and tumorigenic capabilities of glioma cells by regulating the expression of receptor tyrosine kinase AXL.
High ARL2 expression is associated with Osteosarcoma.
conclude that the TBCD*ARL2*beta-tubulin complex represents a functional intermediate in the beta-tubulin folding pathway whose activity is regulated by the cycling of nucleotides on ARL2
Results identified ARL2 and TBCD, as important in tubulin folding and microtubule dynamics. Both ARL2 and TBCD also localize to centrosomes. A growing body of evidence also has found roles for ARL2 inside mitochondria, as a regulator of mitochondrial fusion, and in the traffic of farnesylated cargos between membranes and specifically to cilia and photoreceptor cells. [review]
In conclusion, our study revealed that miR-214 acts as a tumor suppressor via inhibiting proliferation, migration and invasion of cervical cancer cells through targeting ARL2, and that both miR-214 and ARL2 may serve as prognostic or therapeutic targets for cervical cancer.
Novel Biochemical and Structural Insights into the Interaction of Myristoylated Cargo with Unc119 Protein and Their Release by Arl2/3.
We hypothesize that ARL2 plays essential roles inside mitochondria along with other cellular functions, at least in part to provide coupling of regulation between these essential cell processes.
MiR-195 regulates cell apoptosis in a context-dependent manner through directly targeting ARL2.
The G proteins Arl2 acts in a GTP-dependent manner as allosteric release factors for farnesylated cargo.
a novel function of miR-16 targeting ARL2 in modulating proliferation and cell cycle progression.
Data show that bovine and human TBCD have functionally identical roles in tubulin heterodimer assembly, and that the inability of human TBCD to disrupt microtubule integrity can be overcome by siRNA-mediated suppression of expression of Arl2.
C. elegans evl-20 gene encodes a functional homolog of human ARL2. Elimination of evl-20 function results in abnormal vulval, gonad, and male tail development and disrupts embryonic proliferation, hypodermal enclosure, and elongation.
Arl2 is present in centrosomes and propose that its action in regulating tubulin polymerization is mediated at centrosomes
In summary, alterations in Arl2 protein content were found to be associated with modifications in tubulin pools, microtubule dynamics as well as cell cycle progression.
ARL2 and beta-tubulin cofactor D participate in AJC disassembly and epithelial depolarization
Arl2 and Arl3 interactions were characterized.
Arl2 could, via protein phosphatase 2A , influence p53 phosphorylation status.
Crystal structure of the ARL2-GTP-BART complex reveals a novel recognition and binding mode of small GTPase with effector.
two pathways in mitochondria, one affecting ATP levels that is independent of ELMOD2 and the other leading to mitochondrial fusion involving MFN2 that does involve ELMOD2
Studies indicate that Arf-like proteins ARL2 and ARL3 are not substrates for N-myristoyl transferase.
Arl2, a small GTPase, has an important regulator of breast tumor cell aggressivity, both in vitro and in vivo
Arf-like protein 2 interaction with PDEdelta is dependent on GTP, and the binding of PDEdelta substantially stabilizes GTP binding; data suggests that Arl2/3 are specific regulators of PDEdelta
This gene encodes a small GTP-binding protein of the RAS superfamily which functions as an ADP-ribosylation factor (ARF). The encoded protein is one of a functionally distinct group of ARF-like genes.
ADP-ribosylation factor-like 2
, ADP-ribosylation factor-like protein 2
, ADP-ribosylation-like 2
, arf-like protein 2