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Laminin, an extracellular protein, is a major component of the basement membrane.
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analysis of the caf zebrafish model of MDC1A, which has a mutation in LAMA2
The degenerative muscle phenotype in the zebrafish dystrophic mutant, candyfloss (caf) results from mutations in the laminin alpha2 (lama2) gene.
It was established that the frequency of individuals with the COL13A1 (show COL13A1 ELISA Kits)*D/*D genotype was higher in the senile age period. The LAMA2*I/*D genotype was predisposing to longevity among women.
Using high-throughput technology identify LAMA-2 as a candidate medullary sponge kidney disease biomarker possibly employable in future for the early diagnosis of this disease.
Differential protein expression of collagen IV (show COL4 ELISA Kits), laminin alpha2, and nidogen-1 (show NID1 ELISA Kits) indicated basal lamina remodeling develops in ischemic failing versus nonfailing human hearts.
Next generation sequencing was found to be useful for molecular diagnosis of a confirmed case of merosin deficient congenital muscular dystrophy.
did not find positive association signals of the four single nucleotide polymorphisms in the LAMA2 and EGR1 (show EGR1 ELISA Kits) 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 ELISA Kits)-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 ELISA Kits) cohort, which indicates that LAMA2 muscular dystrophy should be included in the LGMD2 (show CAPN3 ELISA Kits) nomenclature.
Crystal structure of LAMM L4 domain
These findings provide a mechanistic understanding of LAMA2 muscular dystrophy and establish a strong basis for a potential treatment.
Data show that laminin alpha2beta1gamma1 (Lm211) can inhibit neuregulin 1 (show NRG1 ELISA Kits) type III (Nrg1III) by limiting protein kinase A (PKA) activation, which is required to initiate myelination.
results indicate a novel role for laminin-dystroglycan interactions in the cooperative integration of astrocytes, endothelial cells, and pericytes in regulating the Blood Brain Barrier.
Laminin alpha2-mediated FAK (show PTK2 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) dimers increase in muscle of mice with muscular dystrophy by merosin deficiency.
Overexpression of laminin alpha1 chain that lacks the dystroglycan binding LG4-5 domains in alpha2 chain deficient mice resulted in prolonged lifespan and improved health.
Ku70 (show XRCC6 ELISA Kits) is a regulator of Bax (show BAX ELISA Kits)-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 ELISA Kits))/dy(Pas (show PASK ELISA Kits)). Homozygous animals rapidly developed a progressive muscular dystrophy leading to premature death.
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