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Laminin, an extracellular protein, is a major component of the basement membrane. Additionally we are shipping Laminin Kits (3) and Laminin Proteins (3) and many more products for this protein.
Showing 10 out of 55 products:
Human Monoclonal Laminin Primary Antibody for IHC (p), ELISA - ABIN395519
Rose, Behm, Drgon, Johnson, Uhl: Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score. in Molecular medicine (Cambridge, Mass.) 2010
Show all 5 references for ABIN395519
Human Monoclonal Laminin Primary Antibody for IHC (p), ELISA - ABIN561638
Lemons, Feng, Bennett, Legesse-Miller, Johnson, Raitman, Pollina, Rabitz, Rabinowitz, Coller: Quiescent fibroblasts exhibit high metabolic activity. in PLoS biology 2010
Show all 2 references for ABIN561638
The degenerative muscle phenotype in the zebrafish dystrophic mutant, candyfloss (caf) results from mutations in the laminin alpha2 (lama2) gene.
did not find positive association signals of the four single nucleotide polymorphisms in the LAMA2 and EGR1 (show EGR1 Antibodies) genes with high myopia
By analyzing the gene test we found that compound heterozygous LAMA2 mutation inherited from the parents. One coming from the father was a gross deletion expanding from exon 36 to exon 65. The from the mother was a missense mutation c.1358G>C
This report widens the clinical spectrum of cerebral manifestations related with mutations in LAMA2
Data showed miR (show MLXIP Antibodies)-29a/c as novel regulators of LAMA2 in ependymoma based on miRNA-mRNA covariation and sequence-based target predictions.
This study demonstrates a wide clinical spectrum of LAMA2-related muscular dystrophy and its prevalence in an LGMD2 (show CAPN3 Antibodies) cohort, which indicates that LAMA2 muscular dystrophy should be included in the LGMD2 (show CAPN3 Antibodies) nomenclature.
Crystal structure of LAMM L4 domain
Data find high frequency mutations in LAMA2 protein in hepatocellular carcinoma (HCC (show FAM126A Antibodies)) patients. Its lower expression levels correlate with tumor progression, poor survival and higher chance of cancer recurrence.
2 patients with partial laminin-alpha2 deficiency and atypical phenotypes, one with almost exclusive central nervous system involvement and second with cardiac dysfunction, rigid spine syndrome and limb-girdle weakness; both have 2 heterozygous LAMA2 variants sharing a potentially pathogenic missense mutation c.2461A>C located in exon 18
Genetic association studies identified two pathogenic mutations in the LAMA2 gene in patients with congenital muscular dystrophy.
Homozygous truncating mutations in POMK lead to congenital muscular dystrophies with secondary merosin deficiency, hypomyelination and intellectual disability.
results indicate a novel role for laminin-dystroglycan (show DAG1 Antibodies) interactions in the cooperative integration of astrocytes, endothelial cells, and pericytes in regulating the Blood Brain Barrier.
Laminin alpha2-mediated FAK (show PTK2 Antibodies) activation in podocytes is an important early event in Alport glomerular pathogenesis.
The effects of merosin knockout on alkaline phosphatase activity in the liver of normal and dystrophic mice is reported.
The data of this study suggested that prosurvival Lama (show LAMA1 Antibodies) interactions in the developing postnatal VZ-SVZ germinal zone regulate the ability, or timing, of oligodendrocyte production to occur appropriately.
Levels of both lipid rafts and raft-located acetylcholinesterase (show AChE Antibodies) dimers increase in muscle of mice with muscular dystrophy by merosin deficiency.
Overexpression of laminin alpha1 chain that lacks the dystroglycan (show DAG1 Antibodies) binding LG4-5 domains in alpha2 chain deficient mice resulted in prolonged lifespan and improved health.
Ku70 (show XRCC6 Antibodies) is a regulator of Bax (show BAX Antibodies)-mediated pathogenesis in laminin-alpha2-deficiency muscle cells.
this study identified a novel spontaneous mouse model of human congenital muscular dystrophy with laminin alpha2 chain deficiency, named dy(Pas (show PASK Antibodies))/dy(Pas (show PASK Antibodies)). Homozygous animals rapidly developed a progressive muscular dystrophy leading to premature death.
merosin contributes to muscle passive stiffness, viscoelasticity, and contractility
Data show that merosin deficiency reduces fatigue and prolongs the duration of force potentiation in sternohyoid muscle from an animal model of merosin-deficient congenital muscular dystrophy.
Laminin, an extracellular protein, is a major component of the basement membrane. It is thought to mediate the attachment, migration, and organization of cells into tissues during embryonic development by interacting with other extracellular matrix components. It is composed of three subunits, alpha, beta, and gamma, which are bound to each other by disulfide bonds into a cross-shaped molecule. This gene encodes the alpha 2 chain, which constitutes one of the subunits of laminin 2 (merosin) and laminin 4 (s-merosin). Mutations in this gene have been identified as the cause of congenital merosin-deficient muscular dystrophy. Two transcript variants encoding different proteins have been found for this gene.
laminin alpha 2 subunit
, laminin, alpha 2 (merosin, congenital muscular dystrophy)
, laminin, alpha 2
, laminin alpha 2 chain
, unm teg15a
, unm tk209
, laminin subunit alpha-2-like
, laminin M chain
, laminin subunit alpha-2
, laminin-12 subunit alpha
, laminin-2 subunit alpha
, laminin-4 subunit alpha
, merosin heavy chain
, dystrophia muscularis