Browse our EPS8 Proteins (EPS8)

Human Epidermal Growth Factor Receptor Pathway Substrate 8 (EPS8) interaction partners

1. we focused on EPS8 because its expression had the greatest impact on patient prognosis (overall survival, p < 0.0001). Overexpression of EPS8 was detected in PDAC clinical specimens. Knockdown assays with siEPS8 showed that its overexpression enhanced cancer cell proliferation, migration, and invasion

2. Eps8 is involved in tumor invasion but not necessarily the development of regional lymph node metastasis

3. Comparative analyses revealed that Eps8 protein was abundant in exosomes derived from metastatic pancreatic tumors and ascites and that the amount of exosomal Eps8 was quantitatively correlated with the in vitro cell migratory activity.

4. Data showed that chronic myeloid leukemia (CML) patients expressed a higher level of EPS8 mRNA in bone marrow mononuclear cells. Functional results revealed that EPS8 regulated multiple biological functions such as proliferation, apoptosis, cell cycle, drug sensitivity of CML cells possibly by mediating the regulation of the BCR-ABL/AKT/mTOR signalling pathway.

5. These results indicate that plasma-membrane-associated PTK6 phosphorylates Eps8, which promotes cell proliferation, adhesion, and migration

6. Eps8/Abi1/Sos1 tricomplex acts as a key molecular switch altering the balance between Rac1 and Rho activation; its presence or absence in pancreatic ductal adenocarcinoma cells modulates alphavbeta6-dependent functions, resulting in a pro-migratory (Rac1-dependent) or a pro-TGF-beta1 activation (Rho-dependent) functional phenotype

7. Immunohistochemistry revealed that Eps8 was significantly increased in cervical cancer specimens compared with squamous intraepithelial lesion and normal cervical tissues. Additionally, it was revealed that Eps8 expression not only correlated with cervical cancer progression, but also exhibited a close correlation with the epithelialmesenchymal transition (EMT) markers, Ecadherin and vimentin.

8. Eps8 is required for continuous membrane blebbing.

9. Erk activity promotes actin bundling by Eps8 to enhance cortex tension and drive the bleb-based migration of cancer cells under non-adhesive confinement.

10. Eps8 is a crucial mediator of Src- and FAK-regulated processes.

11. Eps8 is overexpressed in human breast cancers, possibly by regulating ERK signaling, MMP9, p53 and EMT-like transition to affect breast cancer cell growth, migration and invasion.

12. EPS8, as MDR1 and WT1, may be a clinically valuable biomarker for assessing the outcome of ALL patients.

13. These results indicate that employing the native and modified epitopes identified here in Eps8-based immunotherapy for HLA-A2.1 positive cancer patients may result in efficient anticancer immune responses for diverse tumor types.

14. determined the alpha-synuclein-binding domain of beta-III tubulin and demonstrated that a short fragment containing this domain can suppress alpha-synuclein accumulation in the primary cultured cells

15. The ITSN2 interacts with Eps8 and stimulates the degradation of Eps8 proteins.

16. EPS8 is an F-actin capping and bundling protein. Mutant mice lacking EPS8 (Eps8-/- mice), which is present in the hair bundle, the sensory antenna of the auditory sensory cells that operate the mechano-electrical transduction

17. Eps8 functions as a key coordinator in the interplay between FGFR signalling and trafficking.

18. results suggest that Eps8 may serve as a prognostic factor of responsiveness to chemotherapy in AML patients

19. Novel binding partners and differentially regulated phosphorylation sites clarify Eps8 as a multi-functional adaptor.

20. Eps8 is frequently expressed in OSCC. The aberrant expression of Eps8 closely correlated with poor survival in patients with OSCC.

Mouse (Murine) Epidermal Growth Factor Receptor Pathway Substrate 8 (EPS8) interaction partners

1. Scrutinized the motility of Hnrnpab(-/-) cells and confirmed that the decreases in both cell motility and Eps8 are restored by ectopically coexpressing both alternatively spliced Hnrnpab isoforms, therefore these variants are surprisingly nonredundant for cell motility.

2. Absence of Eps8 produces a weaker phenotype in vestibular hair cells compared to cochlear inner hair cells, since it affects the hair bundle morphology but not the basolateral membrane currents. This difference is likely to explain the absence of obvious vestibular dysfunction in Eps8 knockout mice.

3. Results implicate N-methyl-d-aspartate receptor hyperfunction in the cognitive deficits observed in Epidermal growth factor receptor substrate 8 (Eps8) knockout mice and demonstrate a novel role for Eps8 in regulating hippocampal long-term synaptic plasticity and cognitive function.

4. These findings demonstrate a novel role for Wnt-Dvl1 signalling through Eps8 in the regulation of axonal remodeling.

5. It shows that EPS8, a signaling adapter regulating actin dynamics, is a novel partner of VE-cadherin and is able to modulate YAP activity.

6. The actin-binding proteins eps8 and gelsolin have complementary roles in regulating the growth and stability of mechanosensory hair bundles of mammalian cochlear outer hair cells.

7. These results reveal a previously unknown cell type-specific expression pattern of endogenous Eps8 protein in the mouse hippocampus.

8. the key role of Eps8 actin-capping activity in spine morphogenesis and plasticity and indicate that reductions in actin-capping proteins may characterize forms of intellectual disabilities associated with spine defects.

9. identified Eps8 as a unique actin capping protein specifically required for Dendritic cell migration

10. epidermal growth factor receptor pathway substrate 8 is critical in coordinating the development and functionality of mammalian auditory hair cells

11. critical role for JNK2 and EPS8 in receptor tyrosine kinase signaling and trafficking to convey distinctly different effects on cell migration.

12. It was concluded that MyoXVa, whirlin, and Eps8 are integral components of the stereocilia tip complex, where Eps8 is a central actin-regulatory element for elongation of the stereocilia actin core.

13. Eps8 has a role in preventing intestinal defects and improved metabolic status in mice

14. IRSp53, through its interaction with Eps8, not only affects cell migration but also dictates cellular growth in cancer cells.

15. Eps8 is recruited into a multimolecular signaling complex by Abi1

16. results highlight a critical role for p97(Eps8) in trichostatin A-exerted growth inhibition of v-Src-transformed cells

17. multifaceted role for this complex in actin dynamics, possibly through the participation in alternative larger complexes.

18. Eps8 plays multiple roles in modulating actin filament organization, possibly through its interaction with distinct sets of actin regulatory complexes

19. Expression of eps 8 and tgfbeta 1i4 (signal molecules of epidermal growth factor [EGF] or transforming growth factor-beta [TGF-beta]) showed upregulation. TGF-beta and EGF signal pathways are indicated in O. viverrini-driven cell proliferation.

20. Results report that mice lacking Eps8, a regulator of actin dynamics, are resistant to some acute intoxicating effects of ethanol and show increased ethanol consumption.

Pig (Porcine) Epidermal Growth Factor Receptor Pathway Substrate 8 (EPS8) interaction partners

1. the SSC5:60296617 SNP may affect teat number by regulating the interaction of EPS8 and RAPGEF1 and, finally, affecting the mammogenesis of pigs

2. Coexpression of ezrin with Eps8 promotes the formation of membrane ruffles and tufts of microvilli, whereas expression of ezrin and Eps8L1a induces the clustering of actin-containing structures at the cell surface.