Browse our anti-Family with Sequence Similarity 3, Member B (FAM3B) Antibodies

Human Family with Sequence Similarity 3, Member B (FAM3B) interaction partners

1. FAM3B overexpression contributes to increased resistance to cell death and tumor growth in nude mice.

2. Data suggest that serum PANDER levels are significantly elevated in patients with long-standing type 2 diabetes as compared to patients with recently diagnosed type 2 diabetes and control subjects; serum PANDER levels vary according to degree of insulin (show INS Antibodies) resistance.

3. Circulating level of pancreatic-derived factor (PANDER) in relation to the accumulation in metabolic syndrome suggested that persons with elevated levels of PANDER were associated with an increased risk of metabolic syndrome.

4. in-vitro and in-vivo glucose is a potent stimulator of the PANDER promoter within the liver and this response may be facilitated by ChREBP (show MLXIPL Antibodies).

5. beta-cell-secreted PANDER regulated the hepatic insulin (show INS Antibodies) and lipogenenic signaling and impact overall glycemia.

6. our studies demonstrated that silencing FAM3B promoted p53 (show TP53 Antibodies) phosphorylation and induced p53 (show TP53 Antibodies) accumulation by decreasing Mdm2 (show MDM2 Antibodies) expression, which resulted in apoptotic cell death.

7. These results suggest that FAM3B-258 promotes colon cancer cell invasion and metastasis through upregulation of Slug.

8. Helices B and C and the second disulfide bond of PANDER are essential for PANDER-induced beta-cell death.

9. PANDER is secreted from 2 types of pancreatic cells, glucose stimulates its secretion in beta cell and primary islets but not in alpha-cells, it is likely cosecreted with insulin (show INS Antibodies), and structure and conformation is vital for PANDER secretion.

Mouse (Murine) Family with Sequence Similarity 3, Member B (FAM3B) interaction partners

1. these findings indicate that intestinal L cells are responsive to PANDER, and elevated PANDER levels impair GLP-1 (show GCG Antibodies) production in vitro and in vivo.

2. PANDER strongly impacts hepatic lipid metabolism across metabolic states and may induce a selective hepatic insulin resistant phenotype via the LXR pathway.

3. in-vitro and in-vivo glucose is a potent stimulator of the PANDER promoter within the liver and this response may be facilitated by ChREBP (show MLXIPL Antibodies).

4. F3MB(PANDER) decreases mice hepatic triglyceride and is associated with decreased DGAT1 (show DGAT1 Antibodies) expression

5. X-ray crystal structure of the mouse FAM3B protein.

6. these results demonstrated that the JNK (show MAPK8 Antibodies)-mediated signaling mechanism of palmitic acid -induced beta-cell apoptosis involves up-regulated expression of PANDER and activation of caspase-3 (show CASP3 Antibodies).

7. Data suggest a new link between the endocrine and immune systems and provide useful information for further investigating the physiological functions of PANDER and its involvement in inflammation-related pancreatic disorders.

8. Palmitic acid induces the expression of PANDER and the apoptosis of beta-TC3 cells while glucagon-like peptide-1 (show GCG Antibodies) counteracts the above effects through an activation of Akt (show AKT1 Antibodies) signaling.

9. PANDER promotes lipogenesis and compromises insulin (show INS Antibodies) signaling in the liver by increasing FOXO1 (show FOXO1 Antibodies) activity.

10. Findings further indicate PANDER impacts glycemic levels and may represent a potential but complicated therapeutic target.