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Catalog Number: (IC15581380)
Supplier: MP Biomedicals
Description: A flavanone glycoside with neuroprotective and antioxidant properties. Does not inhibit oral carcinogenesis in a rat model unlike other citrus flavanones, but does exert a protective effect against gastritis and gastric lesions.

SDS


Catalog Number: (10474-936)
Supplier: Bioss
Description: Clefts of the oral-facial region usually occur in early fetal development and can affect the lip, the soft palate (the soft tissue in the back of the mouth) and the hard palate (the roof of the mouth). Cleft lip (with or without cleft palate) is a genetically complex birth defect that occurs in approximately one in every 750-1,000 live births. This is one of the most common birth defects and is multifactorial, with both genetic and environmental causes. Cleft lip- and palate-associated transmembrane protein 1 (CLPTM1) belongs to a family of cleft lip and palate transmembrane proteins. This family also contains cisplatin resistance-related protein (CRR9), which is involved in CDDP-induced apoptosis. The CLPTM1 protein shows strong homology to two Caenorhabditis elegans genes.


Catalog Number: (10285-916)
Supplier: Bioss
Description: Dyskerin (NAP57) associates with the chaperone protein Nopp140 and forms a small ribonucleoprotein particle with GAR1 (NOLA1), NHP2 (NOLA2) and Nop10 for the isomerization of uridine to pseudouridine (1). GAR1, NHP2 and dyskerin localize to the dense fibrillar component of the nucleolus and in nuclear Cajal bodies (2). The dyskerin gene maps to chromosome Xq28 (3). Missense mutations in the dyskerin gene interfere with normal nuclear localization of dyskerin and cause Dyskeratosis congenita (DKC) (4). DKC is a rare, X-linked bone marrow disorder characterized by cutaneous hyperpigmentation, dystrophy of the nails, atrophy of the testicles and leukoplakia of the oral mucosa. The GAR1 gene maps to chromosome 4q25 (5,6). The NHP2 gene maps to chromosome 5q35.3 and encodes a 155-amino acid protein (2,7).


Catalog Number: (77438-574)
Supplier: Bioss
Description: This gene belongs to the Ras oncogene family, whose members are related to the transforming genes of mammalian sarcoma retroviruses. The products encoded by these genes function in signal transduction pathways. These proteins can bind GTP and GDP, and they have intrinsic GTPase activity. This protein undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Mutations in this gene cause Costello syndrome, a disease characterized by increased growth at the prenatal stage, growth deficiency at the postnatal stage, predisposition to tumor formation, mental retardation, skin and musculoskeletal abnormalities, distinctive facial appearance and cardiovascular abnormalities. Defects in this gene are implicated in a variety of cancers, including bladder cancer, follicular thyroid cancer, and oral squamous cell carcinoma. Multiple transcript variants, which encode different isoforms, have been identified for this gene. [provided by RefSeq, Jul 2008]


Catalog Number: (10481-338)
Supplier: Bioss
Description: Serine protease which hydrolyzes a range of proteins including type I collagen, fibronectin and fibrinogen. Can also activate urokinase-type plasminogen activator with low efficiency. May play a specialized role in matrix remodeling processes in liver. Required to sense iron deficiency. Overexpression suppresses activation of the HAMP promoter.Involvement in disease:Defects in TMPRSS6 are the cause of iron-refractory iron deficiency anemia (IRIDA); also known as hypochromic microcytic anemia with defect in iron metabolism or hereditary iron-handling disorder or pseudo-iron-deficiency anemia. Key features include congenital hypochromic microcytic anemia, very low mean corpuscular erythrocyte volume, low transferrin saturation, abnormal iron absorption characterized by no hematologic improvement following treatment with oral iron, and abnormal iron utilization characterized by a sluggish, incomplete response to parenteral iron.


Supplier: Adipogen
Description: Potent, selective and orally available NLRP3 inflammasome inhibitor. Blocks the release of IL-1beta in macrophages primed with LPS and activated with ATP or nigericin, but it does not inhibit NLRP1, NLRC4, AIM2, TLR2 signaling or priming of NLRP3. Prevents oligomerization of ASC in cells stimulated with LPS and nigericin. Active in vivo, blocking the production of IL-1beta and enhancing survival in mouse models of multiple sclerosis and cryopyrin-associated periodic syndrome (CAPS). Also active in ex vivo samples from individuals with Muckle-Wells syndrome. Potential therapeutic agent for NLRP3-associated syndromes, including autoinflammatory and autoimmune diseases.

Supplier: Biotium
Description: This antibody recognizes a glycoprotein of 75 kDa, identified as low affinity Nerve Growth Factor (NGF) Receptor (p75NGFR) or Neurotrophin Receptor (p75NTR). NGFR is expressed in various neural crest cells and their tumors such as melanocytes, melanomas, neuroblastomas, pheochromocytomas and neurofibromas. Reportedly, anti-NGFR is a reliable marker for desmoplastic and neurotropic melanomas. NGFR is expressed in mature non-neural cells such as perivascular cells, dental pulp cells, lymphoidal follicular dendritic cells, basal epithelium of oral mucosa and hair follicles, prostate basal cells, and myoepithelial cells. Anti-NGFR stains the myoepithelial cells of breast ducts and intra-lobular fibroblasts of breast ducts.

CF® dyes are Biotium's next-generation fluorescent dyes. CF®594 is a deep red fluorescent dye (Ex/Em 593/614 nm). It yields the brightest conjugates among spectrally similar dyes, and has excellent photostability.

Catalog Number: (10669-308)
Supplier: Bioss
Description: The cystatin superfamily is a well-established family of cysteine protease inhibitors. Cystatins A and B (type 1) are mainly intracellular; cystatins C, D, E/M, F, G, S, SN and SA cystatins are extracellular (type 2); and the kininogens are type 3 cystatins which are intravascular proteins. All true cystatins inhibit cysteine peptidases of the papain family, such as cathepsins, and some also inhibit legumain family enzymes. Cystatin SA, cystatin S and cystatin SN are found primarily in saliva. Cystatin S and SN can also be expressed in tears, urine and seminal fluid. Cystatin C is a related protein which is expressed in brain, thymus, ovary, epididymis and vas deferens. Cystatin D protects against proteinases in the oral cavity, while Cystatin E/M and F moderate the inhibition of cathepsin proteins. The fetuins, part of the cystatin superfamily, are secretable proteins that influence osteogenesis and bone resorption, regulation of the insulin and hepatocyte growth factor receptors and the response to systemic inflammation. High molecular weight kininogen (Kininogen HC) and low molecular weight kininogen (Kininogen LC) have varied roles, though they both inhibit the thrombin- and plasmin-induced aggregation of thrombocytes.


Catalog Number: (10269-136)
Supplier: Bioss
Description: SRPX2 is a 465 amino acid secreted protein expressed in neurons of the brain, including the rolandic area. It has been suggested that SRPX2 enhances cell motility, migration and adhesion through FAK signaling in gastric and other cancer cells. Localized to the cytoplasm, SRPX2 is a ligand for uPAR (urokinase plasminogen activator), a receptor that is a crucial component of the extracellular plasminogen proteolysis system. SRPX2 may be responsible for rolandic seizures (RSs) associated with oral and speech dyspraxia and mental retardation (MR). The involvement of SRPX2 in these disorders suggests an important role for SRPX2 in the perisylvian region critical for language and cognitive development.


Catalog Number: (89358-520)
Supplier: Genetex
Description: This gene belongs to the Ras oncogene family, whose members are related to the transforming genes of mammalian sarcoma retroviruses. The products encoded by these genes function in signal transduction pathways. These proteins can bind GTP and GDP, and they have intrinsic GTPase activity. This protein undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Mutations in this gene cause Costello syndrome, a disease characterized by increased growth at the prenatal stage, growth deficiency at the postnatal stage, predisposition to tumor formation, mental retardation, skin and musculoskeletal abnormalities, distinctive facial appearance and cardiovascular abnormalities. Defects in this gene are implicated in a variety of cancers, including bladder cancer, follicular thyroid cancer, and oral squamous cell carcinoma. Multiple transcript variants, which encode different isoforms, have been identified for this gene. [provided by RefSeq]


Catalog Number: (75935-044)
Supplier: Rockland Immunochemical
Description: Phosphoribosyl transferase domain containing 1 (PRTFDC1) is highly homologous to the hypoxanthine phosphoribosyltransferase (HPRT1) and may have arisen from a gene duplication event of a common ancestor gene. Recently, it was shown that CpG islands in the PRTFDC1 promoter could be hypermethylated in ovarian cancers and oral squamous-cell carcinomas (OSCC), leading to gene silencing. Restoration of PRTFDC1 expression in OSCC inhibited cell growth in colony-formation assays, while knockdown of PRTFDC1 expression in OSCC that expressed the gene promoted cell growth. These results suggest that PRTFDC1 can act as a tumor-suppressor gene. At least three isoforms of PRTFDC1 are known to exist.


Catalog Number: (10289-176)
Supplier: Bioss
Description: Dyskerin (NAP57) associates with the chaperone protein Nopp140 and forms a small ribonucleoprotein particle with GAR1 (NOLA1), NHP2 (NOLA2) and Nop10 for the isomerization of uridine to pseudouridine (1). GAR1, NHP2 and dyskerin localize to the dense fibrillar component of the nucleolus and in nuclear Cajal bodies (2). The dyskerin gene maps to chromosome Xq28 (3). Missense mutations in the dyskerin gene interfere with normal nuclear localization of dyskerin and cause Dyskeratosis congenita (DKC) (4). DKC is a rare, X-linked bone marrow disorder characterized by cutaneous hyperpigmentation, dystrophy of the nails, atrophy of the testicles and leukoplakia of the oral mucosa. The GAR1 gene maps to chromosome 4q25 (5,6). The NHP2 gene maps to chromosome 5q35.3 and encodes a 155-amino acid protein (2,7).


Catalog Number: (89417-178)
Supplier: Prosci
Description: TMEM16A Antibody: Calcium-activated chloride channels (CaCC) are present in many cell types and mediate physiological functions such as epithelial secretion, sensory signal transduction, and smooth muscle contraction. Subunits of these CaCC's include the transmembrane proteins TMEM16A and TMEM16B. TMEM16A is expressed in epithelial cells of the kidney and lung, pancreas, and sensory neurons and its mRNA is seen in foregut, airway epithelia, and tracheal smooth muscle; mice lacking TMEM16A fail to survive past ten days and show aerophagia and little weight gain. TMEM16A is also overexpressed or amplified in multiple cancers associated with poor survival such as oral cancers and gastrointestinal stromal tumors, suggesting the development of CaCC modulators may be a viable therapeutic strategy.


Catalog Number: (10336-090)
Supplier: Bioss
Description: Apelin is a neuropeptide expressed in the supraoptic and paraventricular nuclei and is an endogenous ligand for APJ, a G protein-coupled orphan receptor which is an alternative coreceptor with CD4 for HIV-1. Apelin and APJ are ubiquitously expressed in peripheral tissues, with highest levels reported for heart and lungs, as well several regions within the central nervous system. The actions of apelin remain largely unknown: Apelin inhibits HIV-1 entry in cells coexpressing CD4 and APJ; the oral intake of Apelin in colostrum and breast milk could have a role in the modulation of the immune responses in neonates; more recent studies have also indicated a role for Apelin in the central control of body fluid homeostasis, by influencing AVP release and drinking behavior. In the cardiovascular system several actions of Apelin have been described, including endothelium-dependent vasodilatation, vasoconstriction through direct action on smooth muscle and positive inotropism.


Catalog Number: (10481-342)
Supplier: Bioss
Description: Serine protease which hydrolyzes a range of proteins including type I collagen, fibronectin and fibrinogen. Can also activate urokinase-type plasminogen activator with low efficiency. May play a specialized role in matrix remodeling processes in liver. Required to sense iron deficiency. Overexpression suppresses activation of the HAMP promoter.Involvement in disease:Defects in TMPRSS6 are the cause of iron-refractory iron deficiency anemia (IRIDA); also known as hypochromic microcytic anemia with defect in iron metabolism or hereditary iron-handling disorder or pseudo-iron-deficiency anemia. Key features include congenital hypochromic microcytic anemia, very low mean corpuscular erythrocyte volume, low transferrin saturation, abnormal iron absorption characterized by no hematologic improvement following treatment with oral iron, and abnormal iron utilization characterized by a sluggish, incomplete response to parenteral iron.


Catalog Number: (76107-400)
Supplier: Bioss
Description: Serine protease which hydrolyzes a range of proteins including type I collagen, fibronectin and fibrinogen. Can also activate urokinase-type plasminogen activator with low efficiency. May play a specialized role in matrix remodeling processes in liver. Required to sense iron deficiency. Overexpression suppresses activation of the HAMP promoter.Involvement in disease:Defects in TMPRSS6 are the cause of iron-refractory iron deficiency anemia (IRIDA); also known as hypochromic microcytic anemia with defect in iron metabolism or hereditary iron-handling disorder or pseudo-iron-deficiency anemia. Key features include congenital hypochromic microcytic anemia, very low mean corpuscular erythrocyte volume, low transferrin saturation, abnormal iron absorption characterized by no hematologic improvement following treatment with oral iron, and abnormal iron utilization characterized by a sluggish, incomplete response to parenteral iron.


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