Secretogranin V (7B2 Protein) (SCG5) ELISA Kits

Mouse (Murine) Secretogranin V (7B2 Protein) (SCG5) interaction partners

1. brain 7B2 can impact Abeta disposition in a manner that facilitates plaque formation.

2. Dynamic modulation of prohormone convertase 2 (PC2)-mediated precursor processing by 7B2 protein has a preferential effect on glucagon synthesis

3. 7B2-related peptides modulate regulated secretion of ACTH in neuroendocrine cells.

4. 7B2 nulls exhibit a multisystem disorder of vital organs, most notably the liver, in which massive steatosis and necrosis are observed. Metabolic derangements in glucose metabolism result in glycogen and fat deposition in liver

5. 7B2 has a role in endoproteolytic processing in mouse brain

6. data indicate that null prohormone convertase 2 and 7B2 protein are not phenotypically equivalent in pituitary proopiomelanocortin (POMC) biosynthesis and granule content

7. Phenotypic differences between the 7B2 and PC2 nulls and play a life-or-death role in the ACTH hypersecretion syndrome present in both 129 nulls.

8. phosphorylation of 7B2 functionally inactivates this protein in a manner analogous to the phosphorylating inactivation of BiP, which impairs its ability to bind substrate

9. Differential expression of 7B2 may contribute to the difference between B6 and C3H mice not only in glucagon production and secretion but also in glucose tolerance.

10. a role for Scg5 in the modulation of body weight

11. 7B2 possesses chaperone activity that blocks partially unfolded pro-PC2 forms from losing catalytic competence and then aggregating.

Human Secretogranin V (7B2 Protein) (SCG5) interaction partners

1. Describe a hereditary mixed polyposis syndrome in which is characterized by SCG5-GREM1 duplication.

2. FAM20C plays a role in 7B2-mediated proPC2 activation by phosphorylating residue Thr111; and that 7B2 function is regulated by alternative splicing.

3. 7B2 chaperones blocked the cytotoxic effects of exogenous hIAPP

4. conclude that 7B2 is a natively disordered protein whose function as an antiaggregant chaperone is likely facilitated by its lack of appreciable secondary structure and tendency to form oligomers

5. data provide insight into novel functions of 7B2 and establish this neural protein as an anti-aggregation chaperone associated with neurodegenerative disease

6. the significant effects of SGNE1/7B2 on the growth and apoptosis of glioblastoma cells provide a first proof for a functional implication of SGNE1/7B2 inactivation in the molecular pathology of gliomas.

7. SGNE1 was overexpressed in gastrointestinal peptide-independent ACTH-independent macronodular adrenal hyperplasia. hyperplasia

8. SGNE1 identified as a novel epigenetically silenced gene in medulloblastomas and its inactivation, as well as its inhibitory effect on tumor cell proliferation and focus formation strongly argues for a significant role in medulloblastoma development.

9. SGNE1 genetic variation does not contribute to obesity and common forms of Type 2 diabetes but may worsen glucose intolerance and insulin resistance, especially in the background of severe and early onset obesity

10. Secretogranins V assays failed to detect increased concentrations in any of the patients with neuroendocrine tumours.