Human Soluble FAM3B/Pancreatic Derived Factor ELISA Kit (DEIA-XY2215)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
serum, EDTA plasma, cell culture supernates
Species Reactivity
Human
Intended Use
This Human soluble Pancreatic Derived Factor/FAM3B ELISA Kit contains the necessary components required for the quantitative measurement of recombinant and/or natural human Pancreatic Derived Factor/FAM3B from cell culture supernates, serum and plasma in a sandwich ELISA format.
Contents of Kit
1. Pancreatic Derived Factor/FAM3B Microplate: 1 plate
2. Pancreatic Derived Factor/FAM3B Standard: 1 vial
3. Detection Antibody-Bitinylated: 1 vial
4. Positive Control: 1 vial
5. Streptavidin HRP Conjugate: 1 vial
6. Dilution Buffer: 1 bottle
7. Antibody Diluent Solution: 1 bottle
8. Wash Buffer: 1 bottle
9. Substrate Solution: 1 bottle
10. Stop Solution: 1 bottle
11. Plate Sealer: 1
12. Plastic Pouch: 1
Storage
2-8°C
Precision
Intra-assay Precision: 4-6%; Inter-assay Precision: 8-10%
Detection Range
6.25-200 ng/mL
Sensitivity
1.5 ng/mL
Standard Curve

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References


FAM3B (PANDER) functions as a co-activator of FOXO1 to promote gluconeogenesis in hepatocytes

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE

Authors: Chi, Yujing; Meng, Yuhong; Wang, Junpei; Yang, Weili; Wu, Zhe; Li, Mei; Wang, Di; Gao, Fangfang; Geng, Bin; Tie, Lu; Zhang, Weiping; Yang, Jichun

FAM3B, also known as PANcreatic DERived factor (PANDER), promotes gluconeogenesis and lipogenesis in hepatocytes. However, the underlying mechanism(s) still remains largely unclear. This study determined the mechanism of PANDER-induced FOXO1 activation in hepatocytes. In mouse livers and cultured hepatocytes, PANDER protein is located in both the cytoplasm and nucleus. Nuclear PANDER distribution was increased in the livers of obese mice. In cultured mouse and human hepatocytes, PANDER was co-localized with FOXO1 in the nucleus. PANDER directly interacted with FOXO1 in mouse and human hepatocytes. PANDER overexpression enhanced PANDER-FOXO1 interaction, and detained FOXO1 in the nucleus upon insulin stimulation in hepatocytes. With the increase in PANDER-FOXO1 interaction, PANDER overexpression upregulated the expression of gluconeogenic genes and promoted gluconeogenesis in both human and mouse hepatocytes. Luciferase reporter assays further revealed that PANDER augmented the transcriptional activity of FOXO1 on gluconeogenic genes. Moreover, PANDER overexpression also interfered the binding of AS1842856, a specific FOXO1 inhibitor, with FOXO1, and impaired its inhibitory effects on gluconeogenic gene expression and gluconeogenesis in hepatocytes. siRNA mediated-silencing of FOXO1 inhibited PANDER-promoted gluconeogenic gene expression and glucose production in hepatocytes. In conclusion, PANDER protein is abundantly present in the nucleus, where it functions as a new co-activator of FOXO1 to induce gluconeogenic gene expression in hepatocytes.

FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p

SCIENTIFIC REPORTS

Authors: Zhang, Wenxiang; Chen, Siyu; Zhang, Zhao; Wang, Chen; Liu, Chang

The proliferation and migration of vascular smooth muscle cells (VSMCs) play an essential role during the development of cardiovascular diseases (CVDs). While many factors potentially contribute to the abnormal activation of VSMCs, hyperglycemia is generally believed to be a major causative factor. On the other hand, FAM3B (named PANDER for its secretory form) is a uniquely structured protein strongly expressed within and secreted from the endocrine pancreas. FAM3B is co-secreted with insulin from the beta-cell upon glucose stimulation and regulates glucose homeostasis. In the present study, we sought to determine the roles of FAM3B in the regulation of VSMC physiology, especially under the hyperglycemic condition. We found that FAM3B expression was induced by hyperglycemia both in vivo and in vitro. FAM3B knockdown inhibited, whereas FAM3B overexpression accelerated VSMC proliferation and migration. At the molecular level, FAM3B inhibited miR-322-5p expression, and enforced expression of miR-322-5p antagonized FAM3B-induced VSMC proliferation and migration, suggesting that FAM3B facilitated VSMC pathological activation via miR-322-5p. Taken together, FAM3B mediates high glucose-induced VSMC proliferation and migration via inhibition of miR-322-5p. Thus, FAM3B may therefore serve as a novel therapeutic target for diabetes-related CVDs.

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