Enzymes

Human USP2 (Ubiquitin-Specific Protease 2) or UPB41, GenBank Accession No. NM_004205, a.a. 259-605(end) with an N-terminal His-tag, MW=40.9 kDa, expressed in an E. coli cell expression system.

Human USP2 (Ubiquitin-Specific Protease 2) or UPB41, GenBank Accession No. NM_004205, a.a. 259-605(end) with an N-terminal His-tag, MW=40.9 kDa, expressed in an E. coli cell expression system.

Superoxide Dismutase 1 (SOD1 or (Cu‐Zn) superoxide dismutase) is the initially discovered mammalian SOD, found in almost all cells, and functioning as an organism’s primary defense against highly toxic reactive oxygen species (ROS). ROS, produced as toxic byproducts of aerobic metabolism, can cause cell damage and apoptosis, and potentially contribute to diseases, including certain heart conditions, degenerative neural diseases, and various oxidative stress and age related disorders. There are three types of mammalian SOD proteins; SOD1, found in the cytoplasm, SOD2 (Mn‐SOD), found in the mitochondria, and SOD3, found in the extracellular space. SOD proteins break down (dismutate) ROS, mainly superoxide, into (non‐toxic) oxygen and (less toxic) peroxide. Subsequently, peroxide is decomposed by other enzymes, most notably, catalase. Various mutations in the SOD1 gene directly correlate with the development of familial amyotrophic lateral sclerosis (FALS) through a yet unknown mechanism.

Superoxide Dismutase 1 (SOD1 or (Cu‐Zn) superoxide dismutase) is the initially discovered mammalian SOD, found in almost all cells, and functioning as an organism’s primary defense against highly toxic reactive oxygen species (ROS). ROS, produced as toxic byproducts of aerobic metabolism, can cause cell damage and apoptosis, and potentially contribute to diseases, including certain heart conditions, degenerative neural diseases, and various oxidative stress and age related disorders. There are three types of mammalian SOD proteins; SOD1, found in the cytoplasm, SOD2 (Mn‐SOD), found in the mitochondria, and SOD3, found in the extracellular space. SOD proteins break down (dismutate) ROS, mainly superoxide, into (non‐toxic) oxygen and (less toxic) peroxide. Subsequently, peroxide is decomposed by other enzymes, most notably, catalase. Various mutations in the SOD1 gene directly correlate with the development of familial amyotrophic lateral sclerosis (FALS) through a yet unknown mechanism.

Human ITGB3 partial ORF (NP_000203.2, 27 a.a. - 136 a.a.) recombinant protein with GST tag at N-terminal.

Human MAFK full-length ORF (BAG52549.1, 1 a.a. - 156 a.a.) recombinant protein with GST tag at N-terminal.

PNLIP is an enzyme which belongs to the lipase family. Secreted from the pancreas, PNLIP is the primary lipase that hydrolyzes dietary fat molecules in the human digestive system, converting triglyceride substrates found in ingested oils to monoglycerides and free fatty acids. Bile salts secreted from the liver and stored in gallbladder are released into the duodenum where they coat and emulsify large fat droplets into smaller droplets, thus increasing the overall surface area of the fat, which allows the lipase to break apart the fat more effectively. The resulting monomers (2 free fatty acids and one 2-monoacylglycerol) are then moved by way of peristalsis along the small intestine to be absorbed into the lymphatic system by a specialized vessel called a lacteal.

Degrades extracellular matrix. Proposed to play a role in breast cancer invasion and metastasis. Exhibits trypsin-like activity as defined by cleavage of synthetic substrates with Arg or Lys as the P1 site.Defects in ST14 are a cause of ichthyosis autosomal recessive with hypotrichosis (ARIH). ARIH is a skin disorder characterized by congenital ichthyosis associated with the presence of less than the normal amount of hair.

HRas, also known as HRAS, belongs to the small GTPase superfamily, Ras family and is widely expressed. It functions in signal transduction pathways. HRas can bind GTP and GDP, and they have intrinsic GTPase activity. It undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS). FCSS is arare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities, tumor predisposition, skin and musculoskeletal abnormalities. Defects in HRAS also can cause congenital myopathy with excess of muscle spindles. HRAS deficiency may be a cause of susceptibility to Hurthle cell thyroid carcinoma. It has been shown that defects in HRAS can cause susceptibility to bladder cancer which is a malignancy