Laminin 111

Injections of this substance are used in treatment for Duchenne muscular dystrophy, and its cellular action may potentially become a focus of study in cancer research.[3] From studying a mouse model, it was found that transcription factors present in the parietal endoderm regulate the expression of the α1 and large amounts of laminin-111 are produced.[5] When the laminin α1 chain is deficient in an organism, an embryo dies, likely as a result of a defective Reichert’s membrane due to a lack of laminin–111 being produced.[5] The injection of laminin-111, however, helps with Duchenne muscular dystrophy, a neuromuscular disease in which the connection between the extracellular matrix and cell cytoskeleton is lost.[6] The experiments utilizing laminin–111 as a source of therapy for Duchenne muscular dystrophy suggest that it has protective qualities in addition to its association with muscle tissue.[13] Focussing on connections between laminin-111 and other proteins involved in cell-to-cell communication could spark further research that may help to further our current understanding of cancer and how to slow down or stop its process.Their study gave the following conclusions: The biological process in which a cell ceases to continue growing and dividing is called quiescence (the opposite of cancer).Decreased expression of laminin-111 and the growth-inhibitory signals that it produces in malignant myoepithelial cells begs for further investigation with regard to cancer research.
A schematic diagram of the structure of laminin 111 and several hypothesized binding sites of cell-surface receptors. [ 1 ]
A schematic diagram of the laminin 111-α6β4 integrin interaction in hemidesmosomes for cell adhesion in epithelial tissue.
proteinlamininisoformsembryonic developmentDuchenne muscular dystrophycancer researchepitheliumkidneytestisovariesblood vesselstranscription factorsendodermReichert’s membraneblastocysttrimermutationsembryobasement membranecell migrationneuromuscular diseaseextracellular matrixcytoskeletonα7-integrinmyoblastdegenerationinflammatory reactionstransplantationcell adhesionproteinscell surface receptorsintegrinsglycoproteinsdystroglycanPI3K/AKT pathwayapoptosispluripotencyembryonic stem cellscytoplasmphosphorylatedGTPaseneuriteNitric Oxidechemical signalsnucleuscancercell differentiationgene transcriptionchromatin remodelingRNA polymerasesU.S. Department of EnergyLawrence Berkeley National Laboratorycytoplasmicquiescenceepithelial cellshomeostaticmalignantmyoepithelial cellstherapeutic