anti-ArfGAP with GTPase Domain, Ankyrin Repeat and PH Domain 2 (AGAP2) Antibodies

Human ArfGAP with GTPase Domain, Ankyrin Repeat and PH Domain 2 (AGAP2) interaction partners

1. The role of AGAP2 in the pro-fibrogenic phenotype of hepatic stellate cells in response to TGFbeta.

2. A pleckstrin homology domain in PIKE-L directly binds alpha-synuclein and antagonizes its aggregation. Accordingly, PIKE-L overexpression decreases dopaminergic cell death elicited by MPP(+), whereas PIKE-L knockdown elevates alpha-synuclein oligomerization and cell death.

3. these findings support that PIKE amplification or overexpression coordinately acts with CDK4 to drive glioblastoma tumorigenesis.

4. Studies showed that overexpression or mutation of PIKE has been observed in a variety of tumors, promoting cancer cell growth, transformation and invasion through AKT signaling or other signaling pathways, such as focal adhesion kinase. [review]

5. Mutation of Fyn phosphorylation sites on PIKE-A, depletion of Fyn, or pharmacological inhibition of Fyn blunts the association between PIKE-A and AMPK, resulting in loss of its inhibitory effect on AMPK.

6. expression of PLC-gamma1 and PIKE positively correlated with the tumor differentiation of oral squamous cell carcinoma.

7. PIKE reduction rescued PI3K-dependent and -independent neuronal defects in fragile X syndrome.

8. In this review the CENTG1 gene is amplified in a variety of human cancers which lead to the enhancement of tumor invasion.

9. AGAP2 plays a role in the signalling and recycling of beta2-adrenergic receptors.

10. Fyn regulates the activity of the adipogenic transcription factor signal transducer and activator of transcription 5a (STAT5a) through enhancing its interaction with the GTPase phosphoinositide 3-kinase enhancer A (PIKE-A).

11. PIKE is highly expressed in human squamous cell carcinoma and has a critical role in EGF-induced squamous cell carcinoma proliferation.

12. The presence of heterogeneous missense mutations of GGAP2 in prostate cancer was associated with aggressive clinical behavior.

13. PIKE is a critical factor in controlling synaptic AMPA receptor insertion.

14. Akt-phosphorylated PIKE-A inhibits UNC5B-induced apoptosis in cancer cell lines in a p53-dependent manner. [PIKE-A]

15. regulates retrograde protein transport between early endosomes and the Golgi complex

16. This study have identified, cloned and characterized PIKE-L, which localizes to both the cytoplasm and the nucleus, activates mGlur1 enhances formation of an mGluRI-Homer-PIKE-L complex, then activates PI3 kinase activity and prevents neuronal apoptosis.

17. a physiologic regulator of Akt and an oncogenic effector of cell invasion

18. PIKE binds PI 3-kinase & stimulates its lipid kinase activity. There are 3 isoforms which function throught the cell and meadiate processes from invasiveness to apoptosis. Review.

19. The AGAP2 colocalized with AP-1, transferrin receptor and Rab4 on endosomes. Overexpression of AGAP2 changed the intracellular distribution of AP-1 and promoted Rab4-dependent fast recycling of transferrin.

20. an important role of PIKE gene aberrations in the molecular pathogenesis of primary glioblastomas

Mouse (Murine) ArfGAP with GTPase Domain, Ankyrin Repeat and PH Domain 2 (AGAP2) interaction partners

1. Dopamine and DOPAC were not changed in 3-mo-old mice but were decreased at 8 mo in the striatum of PIKE-KO mice compared with wild-type mice. DA and DOPAC in hippocampus and substantia nigra were significantly decreased in 3-mo-old and 8-mo-old PIKE-KO mice as compared with wild-type mice. More severe motor defects in PIKE-KO and Fyn-KO mice than in wild-type mice exposed to alpha synuclein and MPTP.

2. Depletion of PIKE-A in C2C12 myotubes diminished the inhibitory activities of TNF-alpha on mitochondrial respiration and lipid oxidation, whereas PIKE-A overexpression exacerbated these cellular responses.

3. PIKE plays pivotal roles to advance oligodendroglia development and myelinogenesis through Akt/mTOR activation.

4. Results demonstrate that the integrity of PIKE signaling is essential for protecting the neurons from excitotoxicity-stimulated damage both in vitro and in vivo.

5. Fyn regulates the activity of the adipogenic transcription factor signal transducer and activator of transcription 5a (STAT5a) through enhancing its interaction with the GTPase phosphoinositide 3-kinase enhancer A (PIKE-A).

6. PIKE is a critical factor in controlling synaptic AMPA receptor insertion.

7. data established the critical role of PIKE in regulating neuronal survival and development by substantiating the PI3K/Akt pathway.

8. PIKE-A is required for prolactin-mediated STAT5a activation in mammary gland development.

9. PIKE knockout mice show augmented lipid oxidation, which is accompanied by enhanced AMPK phosphorylation in muscle and adipose tissue and is implicated in obesity and diabetes development.

10. PIKE-L acts as a downstream survival effector for netrin-1 through UNC5B in the nervous system