Growth Differentiation Factor 3 (GDF3) ELISA Kits

Human Growth Differentiation Factor 3 (GDF3) interaction partners

1. the 4 of the 5 variants in [i]GDF3[/i] gene contribute different pathogenicity in congenital scoliosis, which may provide molecular evidence for clinical genetic testing.

2. OCT4 plays a role as a transcriptional activator for GDF3 transcription in pluripotent human embryonic carcinoma NCCIT cells and contributes to the understanding of the molecular networks of stem cell regulators in germ cell-derived pluripotency and tumorigenesis.

3. The results expand the spectrum of mutations associated with CHDs and first suggest the potentially disease-related GDF3 gene variant in the pathogenesis of CHDs.

4. first evidence that NANOG is a transcriptional activator of the expression of the oncogenic growth factor GDF3 in embryonic carcinoma cells

5. GDF3 expression level was significantly down-regulated in breast cancer tissues compared to the surrounding nontumorous tissues.

6. the conditioned medium from CHO-GDF3 could reduce PC12 cell growth and induce cell differentiation

7. Growth differentiation factor 3 is induced by bone morphogenetic protein 6 (BMP-6) and BMP-7 and increases luteinizing hormone receptor messenger RNA expression in human granulosa cells.

8. Mutation of GDF3 causes ocular and skeletal anomalies.

9. Present data suggested that GDF3 might play important roles in the central nervous system (CNS), especially in cerebral cortex, hippocampus and cerebellum, and it shed new light on further research of GDF3 in the central nervous system.

10. GDF3 regulates both of the two major characteristics of embryonic stem cells: the ability to maintain the undifferentiated state and the ability to differentiate into the full spectrum of cell types.

11. GDF3 regulates adipose-tissue homeostasis and energy balance under nutrient overload in part by signaling through the ALK7 receptor

12. GDF3 is either a bi-functional TGF-beta ligand, or, more likely, that it is a BMP inhibitor that can artificially activate Nodal signaling under non-physiological conditions.

13. GDF3 positivity is helpful in the diagnosis of yolk sac tumor

Mouse (Murine) Growth Differentiation Factor 3 (GDF3) interaction partners

1. Data, including data from studies using knockout mice, suggest that Gdf3-Alk7 axis between adipose tissue macrophages and adipocytes represents previously unrecognized mechanism by which insulin regulates both fat metabolism/lipolysis and adiposity. (Gdf3 = growth differentiation factor-3; Alk7 = activin receptor-like kinase-7)

2. This work establishes PPARgamma as a required metabolic sensor and transcriptional regulator of repair macrophages and establishes GDF3 as a secreted extrinsic effector protein acting on myoblasts and serving as an exclusively macrophage-derived regeneration factor in tissue repair

3. GDF3 has the ability to induce progression of CD24-inducible melanoma in mice.

4. Mice transduced with GDF-3 displayed profound weight gain when fed with high fat diet. The phenotypes included greatly expanded adipose tissue mass, increased body adiposity, highly hypertrophic adipocytes, hepatic steatosis, and elevated plasma leptin.

5. GDF3 regulates both of the two major characteristics of embryonic stem cells: the ability to maintain the undifferentiated state and the ability to differentiate into the full spectrum of cell types.

6. Gdf3 is expressed in the inner cell mass and epiblast, and null mutants frequently exhibit abnormal formation or positioning of the anterior visceral endoderm in pre-gastrulation development

7. Results suggest that GDF1 and GDF3 together represent the functional mammalian homologs of Vg1.

8. GDF3 regulates adipose-tissue homeostasis and energy balance under nutrient overload in part by signaling through the ALK7 receptor

9. GDF3 deficiency selectively affects white adipose through its influence on basal metabolic rates.

Xenopus laevis Growth Differentiation Factor 3 (GDF3) interaction partners

1. Xnr1 and derriere are coexpressed in the posterior paraxial mesoderm at neurula stage, and with Coco define a posttranscriptionally regulated signaling center in the chain leading to an increased TGF-beta signal on the left side of the embryo.