Aperçu des produits pour anti-LRP4 (LRP4) Anticorps

Human Low Density Lipoprotein Receptor-Related Protein 4 (LRP4) interaction partners

1. LRP4 c.2552C>G (p.(T851R) variant was identified in the family with Chiari malformation type 1.

2. A novel splice variant in LRP4 (c.316+1G > A) segregated with Cenani-Lenz syndactyly phenotype in a five generations family.

3. LRP4 mutations alter Wnt (Montrer WNT2 Anticorps)/beta catenin (Montrer CTNNB1 Anticorps) signaling and cause limb and kidney malformations in Cenani-Lenz syndrome.

4. the first evidence suggesting that LRP4 is responsible for the retention of sclerostin (Montrer SOST Anticorps) in the bone environment in humans.

5. study presents 2 sibling fetuses with a prenatal lethal presentation of mesomelic limb reductions, oligosyndactyly, genitourinary malformation and compound heterozygosity for 2 novel truncating mutations in LRP4

6. In Mayer-Rokitansky-Kuster-Hauser syndrome in monoztgotic twins, LRP10 was identified as one of the candidate genes.

7. MuSK (Montrer MUSK Anticorps) myasthenia gravis IgG4 disrupts the interaction of LRP4 with MuSK (Montrer MUSK Anticorps) but both IgG4 and IgG1-3 can disperse preformed agrin (Montrer AGRN Anticorps)-independent AChR clusters

8. LRP4 is essential for maintaining the structural and functional activity of the neuromuscular junction.

9. LRP4 is a new CMS (Montrer Cd2ap Anticorps) disease gene and the 3rd beta propeller domain of LRP4 mediates two signaling pathways in a position-specific manner.

10. [review] Autoantibodies against LRP4 differentially alter neuromuscular transmission, demonstrating how myasthenia gravis can be classified according to the profile of the antibodies; management of myasthenia gravis patients can be adapted accordingly.

Mouse (Murine) Low Density Lipoprotein Receptor-Related Protein 4 (LRP4) interaction partners

1. the serum sclerostin (Montrer SOST Anticorps) levels were strongly increased and the level of sclerostin (Montrer SOST Anticorps) in the tibia was decreased in Lrp4R1170Q/R1170Q mice, confirming the role of LRP4 (Montrer CORIN Anticorps) as an anchor for sclerostin (Montrer SOST Anticorps) in bone.

2. The astrocytic Lrp4 (Montrer CORIN Anticorps) plays an important role in ischemic brain injury response. Lrp4 (Montrer CORIN Anticorps) deficiency in astrocytes seems to be protective in response to ischemic brain injury, likely because of the increased ATP release and adenosine-A2AR (Montrer ADORA2A Anticorps) signaling.

3. LRP4 (Montrer CORIN Anticorps) is expressed by embryonic cortical and hippocampal neurons, and downregulation of LRP4 (Montrer CORIN Anticorps) in these neurons causes a reduction in density of synapses and number of primary dendrites. Collectively, the results demonstrate an essential and novel role of neuronal LRP4 (Montrer CORIN Anticorps) in dendritic development and synaptogenesis in the central nervous system.

4. data suggest a model whereby Lrp4 (Montrer CORIN Anticorps) modulates Wnt (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps) signaling via interaction with Wnt (Montrer WNT2 Anticorps) ligands and antagonists in a context-dependent manner.

5. a critical role for Lrp4 (Montrer CORIN Anticorps), in response to agrin (Montrer AGRN Anticorps), in modulating astrocytic ATP release and synaptic transmission

6. We show that prepatterning in mice requires Lrp4 (Montrer CORIN Anticorps) but not the MuSK (Montrer MUSK Anticorps) Fz-like domain

7. The loss of low density lipoprotein receptor-related protein 4 (Montrer CORIN Anticorps) compromised foetal swallowing and breathing-like movements and downregulated the expression of aquaporin-9 (Montrer AQP9 Anticorps) in the foetal membrane and aquaporin-1 (Montrer AQP1 Anticorps) in the placenta, which possibly affected the amniotic fluid clearance.

8. Reveal novel roles for APP (Montrer APP Anticorps) in regulating neuromuscular synapse formation through hetero-oligomeric interaction with LRP4 (Montrer CORIN Anticorps) and agrin (Montrer AGRN Anticorps) and thereby provide new insights into the molecular mechanisms that govern NMJ formation and maintenance.

9. Results suggest that mdig may contribute to silica-induced lung fibrosis by altering the balance between Th17 and Treg cells.

10. Residues Lys (Montrer LYZ Anticorps)-71, Phe-72 and Gln-73 serve as a novel retention motif in the intracellular pathway to regulate corin (Montrer CORIN Anticorps) cell surface expression and activation.

Cow (Bovine) Low Density Lipoprotein Receptor-Related Protein 4 (LRP4) interaction partners

1. identification of a doublet mutation in complete linkage disequilibrium with syndactyly in one gene of the critical interval: LRP4

2. autosomal recessive loss-of-function mutations in Megf7/Lrp4 result in a form of syndactyly, mulefoot disease

3. 4 new LRP4 non-synonymous missense point mutations co-segregating in Holstein, German Simmental & Simmental-Charolais families represent independent mutations affecting different conserved protein domains.