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anti-Human LRP4 Antibodies:
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Mammalian Monoclonal LRP4 Primary Antibody for ISt, IHC - ABIN1304795
Barik, Lu, Sathyamurthy, Bowman, Shen, Li, Xiong, Mei: LRP4 is critical for neuromuscular junction maintenance. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2014
Show all 5 Pubmed References
Human Polyclonal LRP4 Primary Antibody for ELISA, WB - ABIN451735
Styrkarsdottir, Halldorsson, Gretarsdottir, Gudbjartsson, Walters, Ingvarsson, Jonsdottir, Saemundsdottir, Snorradóttir, Center, Nguyen, Alexandersen, Gulcher, Eisman, Christiansen, Sigurdsson, Kong et al.: New sequence variants associated with bone mineral density. ... in Nature genetics 2008
Human Polyclonal LRP4 Primary Antibody for ICC, IF - ABIN4331498
Pevzner, Schoser, Peters, Cosma, Karakatsani, Schalke, Melms, Kröger: Anti-LRP4 autoantibodies in AChR- and MuSK-antibody-negative myasthenia gravis. in Journal of neurology 2012
LRP4 c.2552C>G (p.(T851R) variant was identified in the family with Chiari malformation type 1.
A novel splice variant in LRP4 (c.316+1G > A) segregated with Cenani-Lenz syndactyly phenotype in a five generations family.
LRP4 mutations alter Wnt (show WNT2 Antibodies)/beta catenin (show CTNNB1 Antibodies) signaling and cause limb and kidney malformations in Cenani-Lenz syndrome.
the first evidence suggesting that LRP4 is responsible for the retention of sclerostin (show SOST Antibodies) in the bone environment in humans.
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
MuSK (show MUSK Antibodies) myasthenia gravis IgG4 disrupts the interaction of LRP4 with MuSK (show MUSK Antibodies) but both IgG4 and IgG1-3 can disperse preformed agrin (show AGRN Antibodies)-independent AChR clusters
LRP4 is essential for maintaining the structural and functional activity of the neuromuscular junction.
LRP4 is a new CMS (show Cd2ap Antibodies) disease gene and the 3rd beta propeller domain of LRP4 mediates two signaling pathways in a position-specific manner.
[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.
pathogenic IgG4 antibodies to MuSK (show MUSK Antibodies) bind to a structural epitope in the first Ig-like domain of MuSK (show MUSK Antibodies), prevent binding between MuSK (show MUSK Antibodies) and Lrp4, and inhibit Agrin (show AGRN Antibodies)-stimulated MuSK (show MUSK Antibodies) phosphorylation.
LRP4 (show CORIN Antibodies) is expressed by embryonic cortical and hippocampal neurons, and downregulation of LRP4 (show CORIN Antibodies) 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 (show CORIN Antibodies) in dendritic development and synaptogenesis in the central nervous system.
data suggest a model whereby Lrp4 (show CORIN Antibodies) modulates Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling via interaction with Wnt (show WNT2 Antibodies) ligands and antagonists in a context-dependent manner.
a critical role for Lrp4 (show CORIN Antibodies), in response to agrin (show AGRN Antibodies), in modulating astrocytic ATP release and synaptic transmission
We show that prepatterning in mice requires Lrp4 (show CORIN Antibodies) but not the MuSK (show MUSK Antibodies) Fz-like domain
The loss of low density lipoprotein receptor-related protein 4 (show CORIN Antibodies) compromised foetal swallowing and breathing-like movements and downregulated the expression of aquaporin-9 (show AQP9 Antibodies) in the foetal membrane and aquaporin-1 (show AQP1 Antibodies) in the placenta, which possibly affected the amniotic fluid clearance.
Reveal novel roles for APP (show APP Antibodies) in regulating neuromuscular synapse formation through hetero-oligomeric interaction with LRP4 (show CORIN Antibodies) and agrin (show AGRN Antibodies) and thereby provide new insights into the molecular mechanisms that govern NMJ formation and maintenance.
Results suggest that mdig may contribute to silica-induced lung fibrosis by altering the balance between Th17 and Treg cells.
These studies demonstrate a role for Lrp4 (show CORIN Antibodies) in hippocampal function.
Lrp4 (show CORIN Antibodies) is a critical player in bone-mass homeostasis.
Data indicate that LRP4 (low-density lipoprotein receptor-related protein 4 (show CORIN Antibodies)) deficiency in bone dramatically elevated serum sclerostin (show SOST Antibodies) levels whereas bone expression of Sost (show SOST Antibodies) encoding for sclerostin (show SOST Antibodies) was unaltered.
identification of a doublet mutation in complete linkage disequilibrium with syndactyly in one gene of the critical interval: LRP4
autosomal recessive loss-of-function mutations in Megf7/Lrp4 result in a form of syndactyly, mulefoot disease
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.
This gene encodes a member of the low-density lipoprotein receptor-related protein family. The encoded protein may be a regulator of Wnt signaling. Mutations in this gene are associated with Cenani-Lenz syndrome.
low-density lipoprotein receptor-related protein 4
, multiple epidermal growth factor-like domains 7
, LDLR dan
, low density lipoprotein receptor-related protein 4
, low density lipoprotein receptor-related protein 4-like
, low-density lipoprotein receptor-related protein 4-like