Attractin (ATRN) ELISA Kits

Human Attractin (ATRN) interaction partners

1. Data indicate that Attractin was involved in male reproduction in both human and BALB/c mice, but it exerted a different expression profile in different species.

2. The levels of both dipeptidyl-peptidase 4 (show DPP4 ELISA Kits) and attractin in circulating monocytes were significantly higher in obese subjects as compared with levels in lean controls or in subjects with type 2 diabetes.

3. It is the first time expression of attractin on monocytes and provide first data suggesting that drugs directed to DP IV-like enzyme activity could affect monocyte function via attractin inhibition.

4. The product of the murine "Mahogany" gene controls energy metabolism and is the murine orthologof human membrane attractin.

5. Through use of PCR from hamster-human somatic cell hybrids, localizes the EST (show MAP3K8 ELISA Kits) AB011120 (KIAA0548) to human chromosome 20p13. AB011120 encodes the central to 3' UTR (show UTS2R ELISA Kits) of the membrane form of human attractin.

6. The product of the murine "Mahogany" locus, controlling agouti-mediated melanocyte pigmentation and control of energy metabolism, is the murine ortholog of human attractin.

7. Provides the genomic basis for production of a soluble and membrane form of attractin by alternative splicing. In the process, by sequencing from positionally-determined BAC clones, confirms the localization of attractin to chromosome 20p13.

Mouse (Murine) Attractin (ATRN) interaction partners

1. Data indicate that Attractin was involved in male reproduction in both human and BALB/c mice, but it exerted a different expression profile in different species.

2. ATRN also has no effect on prion (show PRNP ELISA Kits) disease onset or progression and discuss possible mechanisms that could cause vacuolation of the central nervous system in Mgrn1 and Atrn null mutant mice

3. The age-related Atrn gene progressively loses its function and can cause testis vacuolation and impaired sperm function.

4. the md and mg mutations rescue the A(y) phenotypes by a primarily cAMP-independent mechanism promoting trafficking of MC4R and likely MC1R away from the lysosome toward the cell surface.

5. Over-expression of ATRNL1 (show ATRNL1 ELISA Kits) compensates for loss of ATRN.

6. Atrn is more widely expressed throughout the CNS than previously reported, and expression of Atrn by various cell types suggests that Atrn may serve multiple functions in the CNS.

7. Atrn and dark-like (dal) mutant mice act in a common pathway that is required for normal pigment-type switching and maintenance of cellular integrity.

8. study shows ASIP (show ASIP ELISA Kits)-MC1R (show MSHR ELISA Kits) signaling includes a cAMP-independent pathway through attractin and mahogunin, while the known cAMP-dependent component requires neither attractin nor mahogunin