|1.||Lobel, Peter: 13 articles (03/2014 - 10/2004)|
|2.||Sleat, David E: 10 articles (03/2014 - 10/2004)|
|3.||Sohar, Istvan: 9 articles (03/2014 - 05/2002)|
|4.||Davidson, Beverly L: 5 articles (11/2015 - 10/2004)|
|5.||Crystal, Ronald G: 5 articles (10/2012 - 12/2005)|
|6.||Sondhi, Dolan: 5 articles (10/2012 - 12/2005)|
|7.||Hackett, Neil R: 5 articles (10/2012 - 12/2005)|
|8.||Kim, Kwi-Hye: 4 articles (03/2009 - 10/2004)|
|9.||Passini, Marco A: 4 articles (04/2008 - 10/2004)|
|10.||Lin, L: 4 articles (08/2001 - 07/2000)|
|1.||Neuronal Ceroid-Lipofuscinoses (Neuronal Ceroid Lipofuscinosis)
05/01/2013 - "TPP1, encoding the tripeptidyl-peptidase 1 enzyme, is known as the causative gene for late infantile neuronal ceroid lipofuscinosis disease 2 (CLN2 disease). "
03/01/2013 - "Tripeptidyl-peptidase 1 (TPP1) null or residual activity occurs in neuronal ceroid lipofuscinosis (NCL) with underlying TPP1/CLN2 mutations. "
11/09/2012 - "The classical late infantile neuronal ceroid lipofuscinosis (LINCLs) is an autosomal recessive disease, where the defective gene is Cln2, encoding tripeptidyl-peptidase I (TPP1). "
10/01/2012 - "Late infantile neuronal ceroid lipofuscinosis (LINCL), a fatal, lysosomal storage disorder caused by mutations in the CLN2 gene, results in a deficiency of tripeptidyl-peptidase I (TPP-I) activity in neurons. "
10/01/2012 - "Clinical findings, pathological features and tripeptidyl peptidase 1 (TPP1) activity and genetic mutation analysis data of nine patients affected with the late-infantile form of neuronal ceroid lipofuscinoses (LINCL) in China are systematically reviewed with long-term follow-up. "
05/01/2002 - "In this study, the activities of the lysosomal cysteine proteases cathepsin B and H, dipeptidyl peptidase I, and the serine protease tripeptidyl peptidase I and dipeptidyl peptidase II, all ascribed a role in collagen digestion, were compared with those of the aspartate protease cathepsin D, and lysosomal glycosidases in leukocytes from rheumatoid arthritis patients at different stages of the disease. "
|3.||Neurodegenerative Diseases (Neurodegenerative Disease)
11/11/2015 - "The most common form of the childhood neurodegenerative disease late infantile neuronal ceroid lipofuscinosis (also called Batten disease) is caused by deficiency of the soluble lysosomal enzyme tripeptidyl peptidase 1 (TPP1) resulting from mutations in the TPP1 gene. "
05/01/2013 - "Tripeptidyl peptidase 1 (TPP1) deficiency causes CLN2 disease, late infantile (or classic late infantile neuronal ceroid lipofuscinosis), a paediatric neurodegenerative disease of autosomal recessive inheritance. "
01/01/2010 - "Tripeptidyl aminopeptidase I (TPPI) is a crucial lysosomal enzyme that is deficient in the fatal neurodegenerative disorder called classic late-infantile neuronal ceroid lipofuscinosis (LINCL). "
03/27/2009 - "Late-infantile neuronal ceroid lipofuscinosis (LINCL) is a fatal, incurable neurodegenerative disease of children caused by the loss of the lysosomal protein tripeptidyl-peptidase 1 (TPP1). "
02/06/2009 - "Late infantile neuronal ceroid lipofuscinosis, a fatal neurodegenerative disease of childhood, is caused by mutations in the TPP1 gene that encodes tripeptidyl-peptidase I. We show that purified TPP1 requires at least partial glycosylation for in vitro autoprocessing and proteolytic activity. "
|4.||Lysosomal Storage Diseases (Lysosomal Storage Disease)
04/01/2013 - "LINCL is a uniformly fatal lysosomal storage disease resulting from mutations in the CLN2 gene that encodes for tripeptidyl peptidase 1, a lysosomal enzyme necessary for the degradation of products of cellular metabolism. "
06/18/2004 - "Late-infantile neuronal ceroid lipofuscinosis (CLN2), previously known as the late-infantile form of Batten disease, is a lysosomal storage disease which results from mutations in the gene that codes for tripeptidyl peptidase-I (TPP-I). "
09/01/1999 - "Mutations in tripeptidyl-peptidase I have recently been associated with a lysosomal storage disease, late infantile neuronal ceroid lipofuscinosis."
06/01/2013 - "Infantile and late-infantile neuronal ceroid lipofuscinoses (NCLs) are invariably fatal lysosomal storage diseases associated with defects in lysosomal enzyme palmitoyl-protein thioesterase 1 (PPT-1) or tripeptidyl peptidase 1 (TPP1) activity. "
|5.||Nervous System Heredodegenerative Disorders
06/01/2008 - "Classical late-infantile neuronal ceroid lipofuscinosis (LINCL) is a hereditary neurodegenerative disease of childhood that is caused by mutations in the gene (CLN2) encoding the lysosomal protease tripeptidyl-peptidase I (TPPI). "
01/19/2001 - "The CLN2 gene mutated in the fatal hereditary neurodegenerative disease late infantile neuronal ceroid lipofuscinosis encodes a lysosomal protease with tripeptidyl-peptidase I activity. "
|1.||Serine Proteases (Serine Protease)
|3.||Cysteine Proteases (Cysteine Protease)
|4.||Lysergic Acid Diethylamide (LSD)
|5.||Glycoside Hydrolases (Endoglycosidases)
|9.||Aspartic Acid (Aspartate)
|10.||dipeptidyl peptidase II