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 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.

5. beta-cell-secreted PANDER regulated the hepatic insulin and lipogenenic signaling and impact overall glycemia.

6. It is an important regulator of glucose and lipid metabolism and plays a role in the pathogenesis of nonalcoholic fatty liver disease.(review)

7. our studies demonstrated that silencing FAM3B promoted p53 phosphorylation and induced p53 accumulation by decreasing Mdm2 expression, which resulted in apoptotic cell death.

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

9. Localized to the islets of Langerhans.

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

11. 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, 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 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.

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

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

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

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 counteracts the above effects through an activation of Akt signaling.

9. PANDER promotes lipogenesis and compromises insulin signaling in the liver by increasing FOXO1 activity.

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

11. A paracrine/endocrine effect of insulin on Pander release and a potential glucose-regulatory role for Pander.

12. we provide evidence that identifies PANDER as a regulator of hepatic glucose metabolism, where it amplifies hepatic cAMP and cAMP-response element-binding protein signaling to induce gluconeogenic gene expression and glucose output.

13. Potential role of PANDER in the pancreatic beta-cell for regulation or facilitation of insulin secretion, shown in PANDER knockout mice.

14. In conclusion, Ad-PANDER infection is as effective as truncated recombinant PANDER to induce betaTC3 cell and mouse islet apoptosis.

15. Because FAM3B (PANDER) mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death. (FAM3B)

16. Tissue-specific and glucose-responsive expression of FAM3B promoter were studied.

17. Because PANDER (FAM3B) is expressed by pancreatic beta-cells and in response to glucose in a similar way to those of insulin, PANDER may be involved in glucose homeostasis

18. PANDER is a potential PDX-1 target gene and the A box sites within the promoter region are critical for basal and glucose-stimulated PANDER expression.

19. liver is a target for PANDER, and PANDER may be involved in the progression of diabetes by regulating hepatic insulin signaling pathways.