Browse our anti-Amyloid beta (A4) Precursor Protein-Binding, Family A, Member 2 (APBA2) Antibodies

Human Amyloid beta (A4) Precursor Protein-Binding, Family A, Member 2 (APBA2) interaction partners

1. These results support the hypothesis that APBA2 gene expression in different areas of Alzheimer's patient's brains.

2. Mints are necessary for activity-induced APP and PS1 trafficking and provide insight into the cellular fate of APP in endocytic pathways essential for Abeta production.

3. Aberrant MINT2 methylation in body fluids may predict peritoneal micrometastasis for gastric cancer (GC) patients, which is a potential poor prognostic factor in GC.

4. a significant difference was shown for APBA2 gene expression of peripheral lymphocytes between Chinese Han Tourette syndrome (TS) group and healthy controls idicating the APBA2 gene is a promising peripheral blood biomarker that discriminates between patients with TS and healthy subjects

5. Amyloid beta A4 precursor protein-binding family A member 2 contains a potent neuronal promoter whose activity may be regulated by DNA methylation and glucocorticoid receptor [alpha], paired box protein 5.

6. The co-occurrence of two nonsynonymous mutations in both affected siblings in a single family, each transmitted from a different unaffected parent, suggest a role for APBA2 mutations in rare individuals with ASD.

7. APBA2 were genes activated in early endometrial endometrioid carcinoma (stages I-II).

8. X11beta-mediated reduction in cerebral Abeta is associated with cognition and long-term potentiation in Alzheimer's disease APPswe transgenic mice.

9. Interaction of transcriptional coactivators with Mint1 or Mint2 prevents nuclear localization and transactivation of the transduction network mediated by amyloid precursor protein.

10. The APBA2 gene has been found to map to a more telomeric location in chromosome 15q13 than previously found, and is partially duplicated within the broader region located approximately 5 Mb distal to the intact locus.

11. hXB51 isoforms regulate Abeta generation differently, either enhancing it by modifying the association of X11L with APP or suppressing it in an X11L-independent manner

12. This protein, which is a member of the mammalian LIN-10 protein family and a possible regulator of Abeta production, elevated APP and APLP2 phosphorylation

13. X11alpha and X11beta have roles in beta-amyloid precursor protein processing

14. Comparative genome hybridization suggests a role for NRXN1 and APBA2 in schizophrenia.

15. Phosphorylation of amino acids Ser236 and Ser238 in the X11L regulatory region are critical for increasing association of X11L and amyloid beta-protein precursor and are conserved in X11, a neuronal X11 family protein, but not in non-neuronal X11L2.

Mouse (Murine) Amyloid beta (A4) Precursor Protein-Binding, Family A, Member 2 (APBA2) interaction partners

1. Results indicate that both X11 and X11L exert largely in brain neurons, but X11 may also function in peripheral tissues.

2. Mints 1 and 2 perform redundant synaptic functions and have a role in regulation of gamma-aminobutyric acid release

3. X11beta reduces amyloid beta-protein levels and amyloid plaque formation in the brains of transgenic mice

4. APPPS1 mice are well suited for studying therapeutic strategies and the pathomechanism of amyloidosis by cross-breeding to other genetically engineered mouse models.

5. X11L suppresses the amyloidogenic but not amyloidolytic processing of APP in regions of the brain such as the hippocampus, which express significant levels of X11L.

6. shuttled between the cytoplasm and nucleus, the former more effectively than the latter; leptomycin B (LMB) induced substantial nuclear accumulation of EGFP-X11L

7. X11s associate primarily with APP molecules that are outside of DRM, that the dissociation of APP-X11/X11L complexes leads to entry of APP into DRM, and that cleavage of uncomplexed APP by BACE within DRM

8. This study suggested X11L is involved in the development of neuronal circuits that contribute to conflict resolution.