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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.
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 ELISA Kits).
beta-cell-secreted PANDER regulated the hepatic insulin (show INS ELISA Kits) and lipogenenic signaling and impact overall glycemia.
our studies demonstrated that silencing FAM3B promoted p53 (show TP53 ELISA Kits) phosphorylation and induced p53 (show TP53 ELISA Kits) accumulation by decreasing Mdm2 (show MDM2 ELISA Kits) expression, which resulted in apoptotic cell death.
These results suggest that FAM3B-258 promotes colon cancer cell invasion and metastasis through upregulation of Slug.
Helices B and C and the second disulfide bond of PANDER are essential for PANDER-induced beta-cell death.
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 ELISA Kits), and structure and conformation is vital for PANDER secretion.
PANDER strongly impacts hepatic lipid metabolism across metabolic states and may induce a selective hepatic insulin resistant phenotype via the LXR pathway.
F3MB(PANDER) decreases mice hepatic triglyceride and is associated with decreased DGAT1 (show DGAT1 ELISA Kits) expression
X-ray crystal structure of the mouse FAM3B protein.
these results demonstrated that the JNK (show MAPK8 ELISA Kits)-mediated signaling mechanism of palmitic acid -induced beta-cell apoptosis involves up-regulated expression of PANDER and activation of caspase-3 (show CASP3 ELISA Kits).
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.
Palmitic acid induces the expression of PANDER and the apoptosis of beta-TC3 cells while glucagon-like peptide-1 (show GCG ELISA Kits) counteracts the above effects through an activation of Akt (show AKT1 ELISA Kits) signaling.
PANDER promotes lipogenesis and compromises insulin (show INS ELISA Kits) signaling in the liver by increasing FOXO1 (show FOXO1 ELISA Kits) activity.
Findings further indicate PANDER impacts glycemic levels and may represent a potential but complicated therapeutic target.
A paracrine/endocrine effect of insulin (show INS ELISA Kits) on Pander release and a potential glucose-regulatory role for Pander.
Induces apoptosis of alpha and beta cells in a dose- and time-dependent manner. Present in insulin secretory granules and likely cosecreted with insulin.
family with sequence similarity 3, member B
, cytokine-like protein 2-21
, pancreatic derived factor
, pancreatic-derived factor
, protein FAM3B