anti-Gremlin 2 (GREM2) Anticorps

Zebrafish Gremlin 2 (GREM2) interaction partners

1. Through regulation of bone morphogenetic protein signaling, GREM2 is required for cardiac laterality and atrial differentiation during embryonic development.

2. Gremlin 2 regulates distinct roles of BMP and Endothelin 1 signaling in dorsoventral patterning of the facial skeleton.

3. Prdc is expressed in the developing eyes and the first two pharyngeal arches, in the outer layers of the optic cup, in the arch mesenchyme expands stepwise to the remaining posterior arches, and in the somites and the the swim bladder.

Mouse (Murine) Gremlin 2 (GREM2) interaction partners

1. Grem2 knockdown inhibited cardiomyocyte differentiation, and this effect was similar to that of Notch1 pathway inhibition in vitro. Grem2 enhances the protective effect of cardiac progenitor cells on heart function in a mouse model of myocardial infarction.

2. Grem2 provides a molecular barrier that controls the extent of inflammatory cell infiltration by suppressing BMP2 after myocardial infarction.

3. Grem2 expression is regulated during development and embryonic stem cell differentiation.

4. PRDC binds heparin with high affinity and that heparin binding to PRDC interferes with BMP antagonism.

5. We show that Tbx2 directly represses Grem1 in distal regions of the posterior limb mesenchyme allowing Bone morphogenetic protein (Bmp) signaling to abrogate Fgf4/9/17 expression in the overlying epithelium.

6. Through a combination of biophysical and biochemical studies, the authors determined that PRDC forms biologically active dimers that potently inhibit BMP ligands.

7. The differential regulation of Gremlin2 gene expressions by BMP2 may explain the critical function of these genes during osteoblast differentiation.

8. ovarian PRDC expressed in granulosa cells could be involved in follicular development by antagonizing the actions of theca cell-derived Bone morphogenetic proteins

9. We propose that PRDC might serve as a mediator to antagonize BMP-4 signaling by Wnt.

10. PRDC expression in osteoblasts suppresses differentiation and that reduction of PRDC expression promotes osteogenesis in vitro. PRDC is accordingly identified as a potential novel therapeutic target for the regulation of bone formation.

Human Gremlin 2 (GREM2) interaction partners

1. TT genotype of the rs4454537 polymorphism protective against the development of osteoporosis

2. Our study confirmed that GREM2 is a candidate gene for tooth agenesis, which mutations can explain, however, only a small fraction of the genetic contribution to the pathogenesis of this anomaly.

3. Data show that the GREMLIN 2 (GREM2) expression during Induced Pluripotent Stem Cell (hiPS) cell cardiac differentiation follows the expression pattern of cardiac-specific genes.

4. The structure of Grem2-GDF5 complex has revealed a number of key findings for DAN-family mediated BMP2 inhibition.

5. This study showed that si-Grem2 increased the BMP-2-induced osteogenic differentiation of hBMSCs via the BMP-2/Smad/Runx2 pathway.

6. The present study shows that the Grem2 heparin/HS and BMP2-binding epitopes are unique and independent, where the Grem2-BMP2 complex exhibits a significant increase in binding affinity toward heparin moieties that appear to be partially independent of the Grem2 heparin/HS-binding epitope.

7. Gremlin 2 inhibits adipocyte differentiation through activation of Wnt/beta-catenin signaling

8. mutations associated with tooth malformations

9. GREM2 variants have been identified in atrial fibrillation cohort studies, demonstrating abnormalities in cardiac excitation - supra ventricular tachycardia and atrial fibrillation.

10. The minor allele of rs4454537 is significantly associated with low bone density at the total hip of southern Chinese people. Our study further suggests GREM2 as a novel susceptibility gene for osteoporosis.

11. Through regulation of bone morphogenetic protein signaling, GREM2 is required for cardiac laterality and atrial differentiation during embryonic development.

12. and that a genetic variant in the FMN2/GREM2 locus influences GREM2 expression in osteoblasts and thereby trabecular number and thickness as well as fracture risk.