593 Results for: "Adipogen"

Supplier: Adipogen

Roscovitine-related purine with no activity on CDKs (used as control for roscovitine). Selectively and potently increases production of extracellular Abeta42 and decreases production of extracellular Abeta38 in cultured cells. Extracellular Abeta40 levels remain stable. Intracellular levels of these amyloids appear to remain stable. Alzheimer's Disease (AD) accelerator that interacts with VDAC1, prohibitin and mitofilin, possibly interfering with subcellular compartmentalization and lipid rafts properties, shifting gamma-secretase activity toward Abeta42 generation. Induces a reversible mitochondrial phenotype reminiscent of the one observed in AD brains. Tool to detect inhibitors of Aftin-induced actions (potential anti-AD compounds).

Supplier: Adipogen

Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4). For optimal interaction with LPS, TLR4 requires association with myeloid differentiation protein 2 (MD-2). According to current consensus activation of TLR4 is preceded by the transfer of LPS to membrane-bound (m) or soluble (s) CD14 by LPS-binding protein (LBP). Re-form LPS and lipid A, but not S-form LPS, are capable of inducing TNF-alpha responses also in the absence of CD14. LPS, synthesized by most wild-type (WT) Gram-negative bacteria (S-form LPS), consists of three regions, the O-polysaccharide chain, which is made up of repeating oligosaccharide units, the core oligosaccharide and the lipid A, which harbors the endotoxic activity of the entire molecule. R-form LPS synthesized by the so-called rough (R) mutants of Gram-negative bacteria lacks the O-specific chain. Furthermore, the core-oligosaccharide may be present in different degrees of completion, depending on the class (Ra to Re) to which the mutant belongs. LPS are amphipathic molecules whose hydrophobicity decreases with increasing length of the sugar part. Based upon these differences, S- and R-form LPS show marked differences in the kinetics of their blood clearance and cellular uptake as well as in the ability to induce oxidative burst in human granulocytes and to activate the host complement system.

Supplier: Adipogen

Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4), a member of the highly conserved protein family of TLRs, which are specialised in the recognition of microbial components. In mice, defects in TLR4 result in LPS unresponsiveness. For optimal interaction with LPS, TLR4 requires association with myeloid differentiation protein 2 (MD-2). According to current consensus activation of TLR4 is preceded by the transfer of LPS to membrane-bound (m) or soluble (s) CD14 by LPS-binding protein (LBP). This mechanism is believed to be generally true for LPS signaling. Re-form LPS and lipid A, but not S-form LPS, are capable of inducing TNF-alpha responses also in the absence of CD14. LPS, synthesized by most wild-type (WT) Gram-negative bacteria (S-form LPS), consists of three regions, the O-polysaccharide chain, which is made up of repeating oligosaccharide units, the core oligosaccharide and the lipid A, which harbors the endotoxic activity of the entire molecule. R-form LPS synthesized by the so-called rough (R) mutants of Gram-negative bacteria lacks the O-specific chain. Furthermore, the core-oligosaccharide may be present in different degrees of completion, depending on the class (Ra to Re) to which the mutant belongs. Monophosphoryl Lipid A (MPLA) represents a detoxified derivative of Lipid A and constitutes an important adjuvant in prophylactic and therapeutic vaccines.

Supplier: Adipogen

Human CD11b (alpha M integrin) complexes with CD18 (beta 2 integrin) to form the complement receptor type 3 (CR3) heterodimer which binds to ICAM-1, fibrinogen, C3b and coagulation factor X. CD11b expression is restricted to leukocytes, mainly to myeloid and NK cells.

Supplier: Adipogen

Interleukin-22 (IL-22), also known as IL-10 related T cell derived inducible factor (ILTIF) was initially identified as a gene induced by IL-9 in mouse T cells and mast cells. IL-22 has been shown to activate STAT1 and STAT3 in several hepatoma cell lines and upregulate the production of acute phase proteins. IL-22 is produced by normal T cells upon anti-CD3 stimulation in humans. Mouse IL-22 expression is also induced in various organs upon lipopolysaccharide injection, suggesting that IL-22 may be involved in inflammatory responses. The functional IL-22 receptor complex consists of two receptor subunits, IL-22R (CRF29) and IL-10Rbeta (CRF24), belonging to the class II cytokine receptor family.

Supplier: Adipogen

Receptor for interleukin-33 (IL-33). Its stimulation recruits MYD88, IRAK1, IRAK4 and TRAF6 followed by phosphorylation of MAPK3/ERK1 and/or MAPK1/ERK2, MAPK14 and MAPK8 by similarity. Possibly involved in helper T cell function.

Supplier: Adipogen

Beclin-1 (Bcl-2 interacting coiled-coil protein; ATG6) is a multifunctional protein, well-known as a key regulator of autophagy and required for the initiation step in autophagosome formation. It interacts with several cofactors (Atg14L, UVRAG, Bif-1, rubicon, Ambra1, HMGB1, nPIST, VMP1, SLAM, IP3R, PINK and survivin) to regulate the lipid kinase PI3K protein and promote formation of PIK3C3/VPS34-containing complexes. These interactions induce autophagy, which is a process of programmed cell survival increased during periods of cell stress and extinguished during the cell cycle. Furthermore, beclin-1 is implicated in numerous biological processes, including adaptation to stress, development, endocytosis, cytokinesis, immunity, infection, tumorigenesis, aging and cell death. Beclin-1 is tightly regulated by diverse mechanisms, such as epigenetic silencing, microRNA regulation, post-translational modifications and protein-protein interactions. Multiple diseases are associated with deficiency or malfunction of beclin-1, including cancer and neurodegeneration.

Supplier: Adipogen

Interleukin-4 (IL-4) is a cytokine produced by type 2 helper T cells, the Th2 cells. These cells tends to make a specific set of lymphokines including IL-4, IL-5, IL-6, IL-10, IL-13, IL-3 and GM-CSF and fail to produce IL-2, IFN-gamma, and lymphotoxin (TNF-beta). In addition, mast cells can produce IL-4. IL-4 exerts numerous effects on various hematopoietic cell types. On B cells, IL-4 promotes immunoglobulin class switching to IgE and IgG1 isotypes and upregulates MHC class II and CD23 expression. IL-4 promotes survival, growth, and differentiation of both T and B lymphocytes, mast cells and endothelial cells. In addition, IL-4 inhibits the production of TNF, IL-1, and IL-6 by macrophages.

Supplier: Adipogen

MultimericCD40L™ is a high activity construct in which two trimeric CD40 ligands are artificially linked via the collagen domain of ACRP30. This construct very effectively simulates the natural membrane-assisted aggregation of CD40L in vivo. It provides a simple and equally potent alternative to CD40L+enhancer combinations. MultimericCD40L™ has been shown to suppress alum-induced IL-1beta release and caspase-1 activation in a dose-, CD40- and time dependent manner, without affecting BMDM (Bone marrow-derived macrophages) viability. It also effectively suppressed the inflammasome function triggered by NLRP3 activators. The secretion of caspase-1 independent inflammatory mediators has been shown to be unaltered or even enhanced.

Supplier: Adipogen

CD273 (B7-DC; PD-L2) is a type I surface molecule with homology to CD80, CD86, CD274. It is expressed primarily by dendritic cells and provides a stimulatory signal to CD279 (PD-1; Programmed Cell Death 1) which has an important immunoregulatory role by downregulating the T cell response. CD273 binds to CD279 (PD-1) with a 2-6 fold higher affinity than CD274 and is an important component of immune regulation.

Supplier: Adipogen

Reference compound for the fluorescent (nitric oxide) NO probe DAR-4.

Supplier: Adipogen

NadN (NAD nucleotidase) is a periplasmic enzyme from Haemophilus influenzae, a major pathogen of the respiratory tract in humans that has developed the capability to exploit host NAD(P) for its nicotinamide dinucleotide requirement

Supplier: Adipogen

TIE-2 acts as cell-surface receptor for ANGPT1, ANGPT2 and ANGPT4 and regulates angiogenesis, endothelial cell survival, proliferation, migration, adhesion and cell spreading, reorganization of the actin cytoskeleton, but also maintenance of vascular quiescence. It has anti-inflammatory effects by preventing the leakage of proinflammatory plasma proteins and leukocytes from blood vessels. It is required for normal angiogenesis and heart development during embryogenesis and for post-natal hematopoiesis. After birth, it activates or inhibits angiogenesis, depending on the context. It inhibits angiogenesis and promotes vascular stability in quiescent vessels, where endothelial cells have tight contacts. In migrating endothelial cells that lack cell-cell adhesions, ANGT1 recruits TEK to contacts with the extracellular matrix, leading to the formation of focal adhesion complexes, activation of PTK2/FAK and of the downstream kinases MAPK1/ERK2 and MAPK3/ERK1 and ultimately to the stimulation of sprouting angiogenesis.

Supplier: Adipogen

Sonic hedgehog (Shh) signaling pathway inhibitor. Potential anticancer compound. Cell membrane permeable Smoothened (Smo) antagonist. Acts on extra- and intracellular exposed Smo. Binds to the seven-transmembrane (7TM) pocket. Blocks hedgehog-induced movement of Smo into the primary cilium, disengages Smo-dependent abrogation of Gli2 and Gli3 proteolytic processing and inhibits Gli activity induced by loss of PTCH1.

Supplier: Adipogen

The anti-IgG (human), pAb (HRP) is cross-adsorbed against human IgM and IgA and affinity-purified on pooled human IgG covalently linked to agarose.

Supplier: Adipogen

Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4). For optimal interaction with LPS, TLR4 requires association with myeloid differentiation protein 2 (MD-2). According to current consensus activation of TLR4 is preceded by the transfer of LPS to membrane-bound (m) or soluble (s) CD14 by LPS-binding protein (LBP). Re-form LPS and lipid A, but not S-form LPS, are capable of inducing TNF-alpha responses also in the absence of CD14. LPS, synthesized by most wild-type (WT) Gram-negative bacteria (S-form LPS), consists of three regions, the O-polysaccharide chain, which is made up of repeating oligosaccharide units, the core oligosaccharide and the lipid A, which harbors the endotoxic activity of the entire molecule. R-form LPS synthesized by the so-called rough (R) mutants of Gram-negative bacteria lacks the O-specific chain. Furthermore, the core-oligosaccharide may be present in different degrees of completion, depending on the class (Ra to Re) to which the mutant belongs. LPS are amphipathic molecules whose hydrophobicity decreases with increasing length of the sugar part. Based upon these differences, S- and R-form LPS show marked differences in the kinetics of their blood clearance and cellular uptake as well as in the ability to induce oxidative burst in human granulocytes and to activate the host complement system.

Supplier: Adipogen

NAD synthetase is an essential enzyme involved in both the de novo biosynthesis and salvage of NAD+, catalyzing the final step of both pathways

Supplier: Adipogen

NFATc2 plays a role in the inducible expression of cytokine genes in T cells, especially in the induction of IL-2, IL-3, IL-4, TNF-alpha or GM-CSF. It promotes invasive migration through the activation of GPC6 expression and the WNT5A signaling pathway.

Supplier: Adipogen

The anti-IgG (mouse), pAb (HRP) is cross-absorbed against mouse IgM and IgA, pooled human sera and purified human paraproteins and affinity-purified on pooled mouse IgG covalently linked to agarose.

Supplier: Adipogen

Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4), a member of the highly conserved protein family of TLRs, which are specialised in the recognition of microbial components. In mice, defects in TLR4 result in LPS unresponsiveness. For optimal interaction with LPS, TLR4 requires association with myeloid differentiation protein 2 (MD-2). According to current consensus activation of TLR4 is preceded by the transfer of LPS to membrane-bound (m) or soluble (s) CD14 by LPS-binding protein (LBP). This mechanism is believed to be generally true for LPS signaling. Re-form LPS and lipid A, but not S-form LPS, are capable of inducing TNF-alpha responses also in the absence of CD14. LPS, synthesized by most wild-type (WT) Gram-negative bacteria (S-form LPS), consists of three regions, the O-polysaccharide chain, which is made up of repeating oligosaccharide units, the core oligosaccharide and the lipid A, which harbors the endotoxic activity of the entire molecule. R-form LPS synthesized by the so-called rough (R) mutants of Gram-negative bacteria lacks the O-specific chain. Furthermore, the core-oligosaccharide may be present in different degrees of completion, depending on the class (Ra to Re) to which the mutant belongs. Monophosphoryl Lipid A (MPLA) represents a detoxified derivative of Lipid A and constitutes an important adjuvant in prophylactic and therapeutic vaccines.

Supplier: Adipogen

Fc (human):FasL, Soluble (human) is a high activity construct in which two trimeric FasL are artificially linked via the Fc binding domain of human IgG1. This construct very effectively simulates the natural membrane-assisted aggregation of FasL in vivo. FasL is a cytokine that binds to TNFRSF6/Fas, a receptor that transduces the apoptotic signal into cells. It is involved in cytotoxic T cell mediated apoptosis and in T cell development.

Supplier: Adipogen

Vaspin (Visceral adipose tissue-derived serpin; Serpin A12), a serine protease inhibitor (serpin), is an insulin-sensitizing adipocytokine that has been isolated from both visceral and subcutaneous white adipose tissue. Based on recent findings, vaspin is suggested to regulate immune responses and inflammation and was found to be correlated with various metabolic parameters. Vaspin may represent a novel biomarker for obesity and impaired insulin sensitivity and might serve as a new therapeutic target of metabolic syndrome.

Supplier: Adipogen

The anti-IgG (rat), pAb (R-PE) is cross-adsorbed against pooled mouse sera and pooled mouse plasmacytoma/hybridoma proteins and affinity-purified on pooled rat IgG covalently linked to agarose.

Supplier: Adipogen

DLL1 (Delta-like protein; Delta1) is essential for postnatal arteriogenesis and contributes to tumor progression. DLL1 is involved in differentiation and self-renewal of adipocyte stem cells. Blocks the differentiation of progenitor cells into the B cell lineage while promoting the emergence of a population of cells with the characteristics of a T cell/NK-cell precursor.

Supplier: Adipogen

Irisin is a recently described exercise and PGC1-alpha-induced myokine secreted by skeletal muscle in mice and humans. Irisin has been shown to induce browning of white adipose tissue, but this role has been questioned and a new function in the control of mass and strength of cortical bone has been reported. The membrane fibronectin type III domain containing protein 5 (FNDC5) can be cleaved by an unknown protease to release the Irisin protein (aa 32-143 for human) and potentially also the FNDC5 (extracellular domain, aa 32-153 for human).

Supplier: Adipogen

LYVE-1 has been identified as a major receptor for HA (extracellular matrix glycosaminoglycan hyaluronan) on the lymph vessel wall. Like CD44, the LYVE-1 molecule binds both soluble and immobilized HA. However, unlike CD44, the LYVE-1 molecule colocalizes with HA on the luminal face of the lymph vessel wall and is completely absent from blood vessels. Hence, LYVE-1 is the first lymph-specific HA receptor to be characterized and is a uniquely powerful marker for lymph vessels themselves.

Supplier: Adipogen

GARP (LRRC32) is a ~80kD transmembrane glycoprotein expressed on the cell surface of megakaryocytes, platelets and a subset of activated regulatory T (Treg) cells. It is essential for the surface expression of latent TGF-beta on platelets and activated FOXP3+ regulatory T cells.

Supplier: Adipogen

CD152 and CD28, together with their ligands B7-1 and B7-2, constitute one of the dominant costimulatory pathways that regulate T and B cell responses. CD152 and CD28 are structurally homologous molecules that are members of the immunoglobulin (Ig) gene superfamily. Both CD152 and CD28 are composed of a single Ig V-like extracellular domain, a transmembrane domain and an intracellular domain. CD152 and CD28 are both expressed on the cell surface as disulfide-linked homodimers or as monomers. CD152 was originally identified as a gene that was specifically expressed by cytotoxic T lymphocytes. However, CD152 transcripts have since been found in both Th1 and Th2, and CD4+ and CD8+ T cell clones. Whereas, CD28 expression is constitutive on the surfaces of 95% of CD4+ T cells and 50% of CD8+ T cells and is down regulated upon T cell activation, CD152 expression is upregulated rapidly following T cell activation and peaks approximately 24 hours following activation. Although both CD152 and CD28 can bind to the same ligands, CD152 binds to B71 and B72 with 20-100-fold higher affinity than CD28.

Supplier: Adipogen

Human CD326 is a 40kD glycoprotein expressed on epithelial cells and many carcinomas. It is an adhesion molecule whose function is implicated in carcinogenesis and erythropoesis. CD326 has great potential as a therapeutic and diagnostic marker for cancer.

Supplier: Adipogen

Bmf (Bcl-2-modifying factor) belongs to the Bcl-2 protein family. Bcl-2 family members form hetero- or homo-dimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. Bmf contains a single Bcl-2 homology domain 3 (BH3), and has been shown to interact with other Bcl-2 proteins and functions as an apoptotic activator. Two different start sites can give rise to two proteins of 25 or 30 kDa. It is found to be sequestered to myosin V motors by its association with dynein light chain 2 (DLC2), which may be important for sensing intracellular damage and triggering apoptosis.