AE Binding Protein 1 (AEBP1) ELISA Kits

Human AE Binding Protein 1 (AEBP1) interaction partners

1. this study shows that AEBP1 promotes epithelial-mesenchymal transition of gastric cancer cells by activating the NF-kappaB pathway and predicts poor outcome of the patients

2. The present study elucidates the role of canonical WNT pathway activation by ACLP in NASH pathology, indicating that NASH can be treated by targeting ACLP-induced canonical WNT pathway activation in HSCs.

3. These studies support the conclusion that bi-allelic pathogenic variants in AEBP1 are the cause of this autosomal-recessive Ehlers-Danlos Syndrome subtype.

4. Studies identify ACLP as a stromal derived mediator of adipose progenitor differentiation that may limit adipocyte expansion during white adipose tissue fibrosis.

5. AEBP1 protein is expressed in the pyramidal neurons of human central nervous system and increased in neurons and glial cells of hippocampi and parahippocampal cortices, correlating with the progression of Alzheimer's disease.

6. ACLP stimulates the fibroblast-to-myofibroblast transition by promoting SMA expression via TGFbeta signaling and promoting collagen expression through a TGFbeta receptor-independent pathway.

7. There is no statistically significant differences in the frequency of variants in AEBP1 among the gastroschisis case group compared to a Caucasian control group.

8. Most ACLP knockout mice die perinatally due to abdominal issues.

9. Both cellular proliferation and survival were affected in AEBP1-silenced U87MG and U138MG cell lines and a significant percentage of these cells were directed towards apoptosis.

10. This review focuses on the recently reported regulatory functions that adipocyte enhancer-binding protein 1 (AEBP1) exerts on PPARgamma1 and LXRalpha transcriptional activity in the context of macrophage cholesterol homeostasis and inflammation.

11. Transgenic overexpression of AEBP1 during adipogenesis coupled with a high-fat diet results in massive obesity in female transgenic mice via adipocyte hyperplasia.

12. ACLP and its discoidin-like domain may be novel targets for anti-myofibroblast-based therapies for the treatment of pulmonary fibrosis.

Mouse (Murine) AE Binding Protein 1 (AEBP1) interaction partners

1. The present study elucidates the role of canonical WNT pathway activation by ACLP in NASH pathology, indicating that NASH can be treated by targeting ACLP-induced canonical WNT pathway activation in HSCs.

2. ACLP stimulates the fibroblast-to-myofibroblast transition by promoting SMA expression via TGFbeta signaling and promoting collagen expression through a TGFbeta receptor-independent pathway.

3. Stromal adipocyte enhancer-binding protein (AEBP1) promotes mammary epithelial cell hyperplasia via proinflammatory and hedgehog signaling

4. Data suggest that macrophage AEBP1 plays critical regulatory roles in atherogenesis, and it may serve as a potential therapeutic target for the prevention or treatment of atherosclerosis.

5. Results describe the pathophysiological features of gastroschisis in aortic carboxypeptidase-like protein knockout mice and to characterize the neuromuscular development of the eviscerated intestine.

6. MAPK regulates the transcriptional activity of AEBP1 by a novel dual mechanism, in which MAPK interaction enhances and subsequent phosphorylation decreases the DNA-binding ability of AEBP1

7. Developmental expression pattern is consistent with a regulatory or structural role in the abdominal wall, vasculature, and dermis.

8. AEBP1 plays critical regulatory roles in macrophage cholesterol homeostasis, foam cell formation, and proinflammation.

9. NF-kappaB activity is modulated by means of protein-protein interaction involving AEBP1 and IkappaBalpha.

10. AEBP1 negatively regulates adipose tissue PTEN levels and has a key functional role in modulation of in vivo adiposity.

11. Adipocyte enhancer-binding protein 1 (AEBP1) is up-regulated during monocyte differentiation.

12. ACLP and its discoidin-like domain may be novel targets for anti-myofibroblast-based therapies for the treatment of pulmonary fibrosis.