anti-alpha Actinin 4 (ACTN4) Antikörper

Mouse (Murine) Actinin, alpha 4 (ACTN4) Interaktionspartner

1. Focal segmental glomerulosclerosis Actn4 mutation promotes podocyte detachment through maladaptation to periodic stretch.

2. ACTN4 is a transcriptional coactivator of NF-kappaB (zeige NFKB1 Antikörper).

3. UCHL1 (zeige UCHL1 Antikörper) upregulation in ACTN4-associated FSGS.

4. sLZIP negatively regulates skeletal muscle differentiation via interaction with ACTN4.

5. the C-terminal tail of alpha-actinin-4 is essential for its function in cell migration and adhesion to substratum.

6. Dexamethasone mey protect actin cytoskeleton stabilization from adriamycin-induced podocyte injury via alpha-actinin-4.

7. anti-dsDNA Fab (zeige FANCB Antikörper) may enhance F-actin formation by the proprietary modification of alpha-actinin-4

8. Together, these results indicate that alpha-actinin (zeige ACTN1 Antikörper) and the actin cytoskeleton are important components of the cisternal organelle that are probably required to stabilize the AIS (zeige AR Antikörper).

9. Results suggest that ACTN4 is essential for maintaining normal spreading, motility, cellular and nuclear cross-sectional area, and contractility of lung fibroblasts by maintaining the balance between transcellular contractility and cell-adhesion.

10. newly developed mouse model of ACTN4-associated FSGS suggests a cause-and-effect relationship between actin cytoskeleton dysregulation by mutant alpha-actinin-4 and the deterioration of the nephrin (zeige NPHS1 Antikörper)-supported slit diaphragm complex.

Human Actinin, alpha 4 (ACTN4) Interaktionspartner

1. ACTN4 knockdown resulted in the blockage of malignant cell proliferation, colony formation, and ameliorated metastasis potency. ACTN4-positive CSCs exhibited a higher ESA (zeige FLOT2 Antikörper)(+) proportion, increased mammosphere-formation ability, and enhanced in vivo tumorigenesis ability.

2. These results demonstrate that both actinin (zeige ACTN1 Antikörper)-1 and actinin-4 participate in the assembly of F-actin at invadopodia. Additionally, actinin-4 may have a selective advantage in accelerating invadopodia-mediated invasion of carcinoma cells.

3. Gene amplification of ACTN4 was a significant independent risk factor for death in patients with stage I/II oral tongue cancer (hazard ratio 6.08, 95% confidence interval 1.66-22.27). Gene amplification of ACTN4 is a potential prognostic biomarker for overall survival in oral tongue cancer.

4. ACTN4 knockdown near-completely abrogates both radioresistance and epithelial-mesenchymal transition-associated changes in breast cancer cells.

5. Fascin and alpha-actinin intrinsically segregate to discrete bundled domains that are specifically recognized by other actin-binding proteins.

6. Suggest that ACTN4 as a potential predictive biomarker for efficacy of adjuvant chemotherapy in stage-IB/II patients with non-small cell lung cancer, by reflecting the metastatic potential of tumor cells.

7. High ACTN4 expression is associated with Lung Squamous Cell Carcinoma.

8. Our findings indicate that ACTN4 promotes EMT (zeige ITK Antikörper) and tumorigenesis by regulating Snail (zeige SNAI1 Antikörper) expression and the Akt (zeige AKT1 Antikörper) pathway in cervical cancer. We propose a novel mechanism for EMT (zeige ITK Antikörper) and tumorigenesis in cervical cancer.

9. Study found a functional Validation of an Alpha-Actinin-4 Mutation as a Potential Cause of an Aggressive Presentation of Adolescent Focal Segmental Glomerulosclerosis.

10. SERPINE1 (zeige SERPINE1 Antikörper), ANGPLT4, CCL20 (zeige CCL20 Antikörper), and SAA1 (zeige SAA1 Antikörper) as well as the NF-kappaB (zeige NFKB1 Antikörper) (p65 (zeige GORASP1 Antikörper)) binding sites on GR-transrepressed promoters such as IL-1beta (zeige IL1B Antikörper), IL-6 (zeige IL6 Antikörper), and IL-8 (zeige IL8 Antikörper) Taken together, our data establish ACTN4 as a transcriptional co-regulator that modulates both dexamethasone-transactivated and -transrepressed genes in podocytes.