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Major intrinsic protein is a member of the water-transporting aquaporins as well as the original member of the MIP family of channel proteins. Additionally we are shipping Mitochondrial Intermediate Peptidase Proteins (5) and Mitochondrial Intermediate Peptidase Kits (3) and many more products for this protein.
Showing 10 out of 75 products:
Human Polyclonal MIPEP Primary Antibody for IHC (p), WB - ABIN388246
Marcondes, Torquato, Assis, Juliano, Hayashi, Oliveira: Mitochondrial intermediate peptidase: expression in Escherichia coli and improvement of its enzymatic activity detection with FRET substrates. in Biochemical and biophysical research communications 2010
Show all 2 references for ABIN388246
Human Polyclonal MIPEP Primary Antibody for EIA, IHC (p) - ABIN356963
Chew, Buck, Peretz, Sirugo, Rinaldo, Isaya: Cloning, expression, and chromosomal assignment of the human mitochondrial intermediate peptidase gene (MIPEP). in Genomics 1997
A novel MIP (show TNPO1 Antibodies) frame-shift mutation in familial congenital nuclear cataract patient
defects in AQP-0 (show MIP Antibodies) permeability may be a cause for presbyopia.
the p.D150H mutation is a novel disease-causing mutation in MIP (show TNPO1 Antibodies), which leads to congenital progressive cortical punctate cataract by impairing the trafficking mechanism of AQP0 (show MIP Antibodies).
Authors identified a novel nonsense mutation in MIP (show TNPO1 Antibodies) (c.657 C>G; p.Y219*) (major intrinsic protein gene) that segregates with congenital posterior polar cataract in a Chinese family.
Functional evidence linking the new MIP (show TNPO1 Antibodies) mutation of G215D to autosomal dominant congenital cataracts.
A novel donor splice-site mutation (c.606+1G>A) in the MIP (show TNPO1 Antibodies) gene causes congenital cataract in a Chinese family.
the first nonsense mutation of MIP (show TNPO1 Antibodies) identified in autosomal dominant congenital cataracts
Mutation of this conserved glycine residue leads to improper trafficking of AQP0 (show MIP Antibodies)-G165D and loss of water channel (show AQP4 Antibodies) function.
Aquaporin 0 (show MIP Antibodies) R233K mutation did not affect the expression, location and trafficking of the protein but did influence the interaction between AQP0 (show MIP Antibodies) and CaM (show CALM1 Antibodies).
Direct tissue analysis led to the detection of aging-related AQP0 (show MIP Antibodies) modifications including carbamylation, acetylation, and oleoylation.
The product of this gene performs the final step in processing a specific class of nuclear-encoded proteins targeted to the mitochondrial matrix or inner membrane. This protein is primarily involved in the maturation of oxidative phosphorylation (OXPHOS)-related proteins. This gene may contribute to the functional effects of frataxin deficiency and the clinical manifestations of Friedreich ataxia.
mitochondrial intermediate peptidase
, Mitochondrial intermediate peptidase
, aquaporin 0
, lens fiber major intrinsic protein
, Mitochondrial intermediate peptidase, mitochondrial