anti-Pleiomorphic Adenoma Gene-Like 2 (PLAGL2) Antikörper

Human Pleiomorphic Adenoma Gene-Like 2 (PLAGL2) Interaktionspartner

1. Study results indicated that PLAGL2 was overexpressed in colorectal cancer (CRC) as a protooncogene and that it could active the Wnt/betacatenin pathway as a transcription factor by binding with the promoter region of Wnt6.

2. overexpression of miR-449a inhibited the expression of PLAGL2 significantly and the knockdown of PLAGL2 expression inhibited the breast cancer cell proliferation and metastasis

3. increased expression correlates to prostate cancer progression following radical prostatectomy and may serve as novel poor prognostic marker

4. Our findings indicated that PLAGL2 might be a very upstream key molecule regulating Epithelial-mesenchymal transition involved in Wnt/bcatenin signaling pathway in Colorectal adenocarcinoma

5. Our findings indicate that PALGL2 serves as a tumor oncoprotein in the development and progression of colorectal cancer

6. PLAGL2 expression induces lamellipodia formation and disruption of stress fiber formation.

7. PLAGL2 regulate cell cycle and apoptosis via activation of the p53 family member, p73, in human promonocytic U937 cells.

8. Transcriptome analysis revealed that these differentiation-suppressive activities are attributable in part to PLAGL2 modulation of Wnt/beta-catenin signaling

9. The data identify PC2 as a novel PLAGL2-binding protein and important mediator of PLAGL2 transactivation.

10. PLAGL2 may modulate SP-C expression during lung development.

11. Plag1 and Plagl2 are novel leukemia oncogenes that act by expanding hematopoietic progenitors expressing CbF beta-SMMHC.

12. These data clearly identify PLAGL2 as a novel regulator of NCF2/p67phox gene expression as well as NADPH oxidase activity and contribute to a greater understanding of the transcriptional regulation of NCF2.

13. Coexpression of Tip60 and PLAGL2 completely abolishes the sumoylation of PLAGL2.

14. Nuclear PLAGL2 occupied and transactivated the endogenous SP-C promoter in hypoxic lung cells.These results further suggest that PLAGL2 is an oxidative stress responding regulator in lung cells.

15. This study thus uncovers a novel function of PLAGL2 as an oncoprotein through regulating the stability of Pirh2.

16. These data suggests that Ubc9 can function as a co-factor of PLAGL2, uncoupling from its enzymatic activity, to mediate PLAGL2 interactive SP-C promoter activity.

17. Increased cell injury and/or death could be caused directly by the upregulation of bNip3, a preapoptotic molecule that dimerizes with Bcl-2, or indirectly by the aberrant expression of SP-C-induced endoplasmic reticulum stress in epithelial cells.

Mouse (Murine) Pleiomorphic Adenoma Gene-Like 2 (PLAGL2) Interaktionspartner

1. expression is associated with the development of lung adenocarcinoma and emphysema

2. Transcriptome analysis revealed that these differentiation-suppressive activities are attributable in part to PLAGL2 modulation of Wnt/beta-catenin signaling

3. induces the expression of a proapoptotic protein Nip3, leading to cellular apoptosis.

4. PlagL2 regulates important aspects of dietary lipid absorption, and the PlagL2(-/-) animal model has implications for the amelioration of obesity and the metabolic syndrome.

5. Increased cell injury and/or death could be caused directly by the upregulation of bNip3, a preapoptotic molecule that dimerizes with Bcl-2, or indirectly by the aberrant expression of SP-C-induced endoplasmic reticulum stress in epithelial cells.