diarrhea

Rotavirus A (strain Nebraska calf diarrhea virus) VP7 Protein (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 36.2 kDa and the accession number is P04511.

Bovine viral diarrhea virus (strain SD-1) Genome polyprotein (His) is expressed in Baculovirus insect cells with N-10xHis tag. The predicted molecular weight is 21.4 kDa and the accession number is Q01499.

Bovine viral diarrhea virus (strain SD-1) Genome polyprotein (E. coli, His) is expressed in E. coli expression system with N-10xHis tag. The predicted molecular weight is 25.0 kDa and the accession number is Q01499.

Rotavirus A (strain Nebraska calf diarrhea virus) VP6 Protein (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 50.8 kDa and the accession number is A7J3A1.

Rotavirus A (strain Nebraska calf diarrhea virus) VP4 Protein (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 33.2 kDa and the accession number is P17465.

Spike-forming protein that mediates virion attachment to the host epithelial cell receptors and plays a major role in cell penetration, determination of host range restriction and virulence. Rotavirus attachment and entry into the host cell probably involves multiple sequential contacts between the outer capsid proteins VP4 and VP7, and the cell receptors. It is subsequently lost, together with VP7, following virus entry into the host cell. Following entry into the host cell, low intracellular or intravesicular Ca(2+) concentration probably causes the calcium-stabilized VP7 trimers to dissociate from the virion. This step is probably necessary for the membrane-disrupting entry step and the release of VP4, which is locked onto the virion by VP7.; Forms the spike 'foot' and 'body' and acts as a membrane permeabilization protein that mediates release of viral particles from endosomal compartments into the cytoplasm. During entry, the part of VP5* that protrudes from the virus folds back on itself and reorganizes from a local dimer to a trimer. This reorganization may be linked to membrane penetration.; Forms the head of the spikes and mediates the recognition of specific host cell surface glycans. It is the viral hemagglutinin and an important target of neutralizing antibodies.

Cholera toxin is protein complex secreted by the bacterium Vibrio cholerae. It is responsible for the massive, watery diarrhea characteristic of cholera infection. Cholera enterotoxin subunit B (CTXB) pentameric ring directs the A subunit to its target by binding to the GM1 gangliosides present on the surface of the intestinal epithelial cells. It can bind five GM1 gangliosides. It has no toxic activity by itself.

Staphylococcal enterotoxins cause the intoxication staphylococcal food poisoning syndrome. The illness is characterized by high fever, hypotension, diarrhea, shock, and in some cases death. Enterotoxin type G Protein, S. aureus (strain N315), Recombinant (His) is expressed in yeast with N-6xHis tag. The predicted molecular weight is 29.0 kDa and the accession number is P0A0L7.

LTB (Lymphotoxin Beta) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. Lymphotoxin beta is a type II membrane protein of the TNF family. It anchors lymphotoxin-alpha to the cell surface through heterotrimer formation. Heat-labile enterotoxin B subunit (LTB) of enterotoxigenic Escherichia coli (ETEC) is both a strong mucosal adjuvant and immunogen. It is a subunit vaccine candidate to be used against ETEC-induced diarrhea. It has already been expressed in several bacterial and plant systems.LTB provokes a systemic immune response and exerts adjuvant effects on mucosal immune responses to unrelated antigens. Diseases associated with LTB include Synovitis and Myasthenic Syndrome, Congenital, 2C, Associated With Acetylcholine Receptor Deficiency.

ETHE1, also known as HSCO, is a sulfur dioxygenase that localizes within the mitochondrial matrix. ETHE1 probably plays an important role in metabolic homeostasis in mitochondria. It may also function as a nuclear-cytoplasmic shuttling protein that binds transcription factor RELA/NFKB3 in the nucleus and exports it to the cytoplasm. ETHE1 can suppresses p53-induced apoptosis by preventing nuclear localization of RELA. Mutations in ETHE1 gene result in ethylmalonic encephalopathy. Ethylmalonic encephalopathy is an autosomal recessive, invariably fatal disorder characterized by early-onset encephalopathy, microangiopathy, chronic diarrhea, defective cytochrome c oxidase (COX) in muscle and brain, high concentrations of C4 and C5 acylcarnitines in blood and high excretion of ethylmalonic acid in urine.

Mevalonate kinase belongs to the GHMP kinase family, Mevalonate kinase subfamily. It can be found in a wide variety of organisms from bacteria to mammals. Mevalonate kinase may be a regulatory site in the cholesterol biosynthetic pathway. Defects in mevalonate kinase can cause mevalonic aciduria (MEVA). It is an accumulation of mevalonic acid which causes a variety of symptoms such as psychomotor retardation, dysmorphic features, cataracts, hepatosplenomegaly, lymphadenopathy, anemia, hypotonia, myopathy, and ataxia. Defects in mevalonate kinase can also cause hyperimmunoglobulinemia D and periodic fever syndrome (HIDS). HIDS is an autosomal recessive disease characterized by recurrent episodes of unexplained high fever associated with skin rash, diarrhea, adenopathy (swollen, tender lymph nodes), arthralgias, and/or arthritis.

Staphylococcal enterotoxins cause the intoxication staphylococcal food poisoning syndrome. The illness is characterized by high fever, hypotension, diarrhea, shock, and in some cases death. Enterotoxin type G Protein, S. aureus (strain Mu50/ATCC 700699), Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 43.0 kDa and the accession number is P0A0L6.

Interferon-induced BST2 (bone marrow stromal cell antigen 2) inhibits viral replication by tethering enveloped virions to the cell surface to restrict viral release and by inducing the NFKB-dependent antiviral immune response. BST2 expression was significantly increased during porcine epidemic diarrhea virus (PEDV) infection of Vero cells by IRF1 targeting its promoter. Both the BST2 and N protein interacted with the E3 ubiquitin ligase MARCHF8/MARCH8 and the cargo receptor.

Staphylococcal enterotoxins cause the intoxication staphylococcal food poisoning syndrome. The illness is characterized by high fever, hypotension, diarrhea, shock, and in some cases death. Enterotoxin type G Protein, S. aureus (strain N315), Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 43.0 kDa and the accession number is P0A0L7.

Cholera toxin (CT) produced by Vibrio cholerae causes the devastating diarrhea of cholera by catalyzing the ADP-ribosylation of the alpha subunit of the intestinal Gs protein (Gsalpha), leading to characteristic water and electrolyte losses. Mammalian cells contain ADP-ribosyltransferases similar to CT and an ADP-ribosyl(arginine)protein hydrolase (ADPRH), which cleaves the ADP-ribose-(arginine)protein bond, regenerating native protein and completing an ADP-ribosylation cycle. CT-catalyzed ADP-ribosylation of cell proteins can be counteracted by ADPRH, which could function as a modifier gene in disease. Further, our study demonstrates that enzymatic cross talk exists between bacterial toxin ADP-ribosyltransferases and host ADP-ribosylation cycles. In disease, toxin-catalyzed ADP-ribosylation overwhelms this potential host defense system, resulting in persistence of ADP-ribosylation and intoxication of the cell. Mono-ADP-ribosylation is a reversible modification of proteins with NAD:arginine ADP-ribosyltransferases and ADP-ribosylarginine hydrolases (ADPRH) catalyzing the opposing arms of an ADP-ribosylation cycle. The ADPRH cDNA had been cloned from human, rat, and mouse tissues and high levels of mRNA were found in brain, spleen, and testis. Human ADP-ribosylhydrolase 1 (hARH1, ADPRH) cleaves the glycosidic bond of ADP-ribose attached to an Arg residue of a protein.