28985 Results for: "WS-12&amp"

Supplier: ENZO LIFE SCIENCES

TRMP8 agonist.

Supplier: SURESCREEN

These multipanel drugs tests can detect up to 12 drugs simultaneously.

Supplier: SURESCREEN

The Multi-Cassette only requires a small amount of urine to perform the test, with test results available at 5 minutes. This multiline format test comes with a pipette for an easy-to-use process.

Supplier: SURESCREEN

The multicassette tests for up to 12 several drugs simultaneously, and is very easy to use. The urine sample is added to the sample well with the pipette that comes with the kit, and resuts are read at 3 minutes. Tests are individually wrapped in a foil pouch, to ensure the high-quality of the product is retained throughout the shelf-life.

Supplier: Biosensis

Adenylate cyclases are enzymes which interact with and are activated by the GTP bound alpha subunits of trimeric G-proteins. Activated adenylate cyclases are responsible for the production of the important "second messenger" signalling molecule cyclic-AMP, which is generated from ATP. The type III adenylate cyclase enzyme is localized in the membranes surrounding the cilia in neurons, and our antibody is an excellent marker of neuronal cilia in the brain and in cells in tissue culture. Adenylate cyclase type III is a large complex molecule of, in the human, 1145 amino acids with a deduced molecular weight of 129kDa. The protein may be variably glycosylated, so that on SDS-PAGE and western blots it runs as a diffuse band of about 160kDa in cortex and about 200kDa in olfactory epithelium. The molecule has a complex structure, with 12 transmembrane domains and two cyclase domains. Each cyclase domain is immediately C-terminal to 6 transmembrane segments, but only the second, C-terminal cyclase is believed to be catalytically active.

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterized by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumors (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterized by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumors (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterized by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumors (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterized by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumors (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterized by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumors (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterized by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumors (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterized by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumors (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterized by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumors (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterized by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumors (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterised by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumours (2).

Supplier: Bioss

Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonpeptide that is involved in the regulation of body fluid osmolality (1-3). AVP mediates its effects through a family of G-protein coupled receptors, the vasopressin receptors type V1a, V2 and V3 (also designated V1b) (1,2). The AVP receptor V1a is responsible for several functions, including blood vessel constriction, liver glycogenolysis and platelet adhesion (3). It is detected as a full length protein and a shorter protein, which results from proteolytic cleavage of its amino terminus (4). The V1a receptor is coupled to Gq/11 protein, which increases the intracellular calcium concentration (3). The human AVP receptor V2 gene maps to chromosome Xq28 and is expressed in lung and kidney (5,6). Mutations in the V2 receptor result in nephrogenic diabetes insipidus (NDI), a rare X-linked disorder characterised by the inability of the kidney to concentrate urine in response to AVP (5,7). The AVP Receptor V2 activates the Gs protein and the cyclic AMP second messenger system (7). The AVP receptor V3 is preferentially expressed in the pituitary and stimulates the release of adrenocorticotropic hormone (ACTH) in response to AVP by mobilizing intracellular calcium stores (8). AVP receptor antagonists may have potential therapeutic effects in hypertension, congestive heart failure, nephrotic syndrome and ACTH-secreting tumours (2).

Supplier: VWR Chemicals

5% water has been added to maintain liquidity at room temperature.

Supplier: 3M

The Peltor™ WS™ LiteCom Plus Headset is available in multiple mounting styles, and features an integrated pre-programmed analog two-way radio, Bluetooth® multipoint connectivity, noise-cancelling microphone, and a level-dependent function for ambient listening.

Supplier: 3M

3M™ PELTOR™ WS™ LiteCom Pro III headsets are high-performance hearing protectors with a built-in analogue and digital programmable two-way communication radio, level-dependent functionality for ambient listening, Bluetooth® multipoint connectivity, Lithium-ion rechargeable battery, and an external connection jack. Available in headband, neckband, and helmet-mounted models.

Supplier: 3M

Peltor™ WS™ ProTac XPI is a range of level-dependent Bluetooth® headsets for effective hearing protection without compromising communication. They come in a high visibility yellow colour, with a headband, neckband, or helmet attachment, and are also available with FLX2 accessory connectors.

Supplier: Thermo Fisher Scientific

AMP (2-Amino-2-methylpropanol), (max. 5% H₂O) 95%

Supplier: Thermo Fisher Scientific

AMP (2-Amino-2-methylpropanol) 99%

Supplier: Apollo Scientific

Used for the preparation of buffer solutions, suitable for the determination of alkaline phosphatase.

Supplier: Thermo Fisher Scientific

Adenosine-5'-monophosphoric acid (AMP) 99%

Supplier: 3M

The 3M™ Peltor™ WS™ LiteCom Pro III Headset features an integrated, programmable analog/digital two-way radio, Bluetooth® Multipoint connectivity, noise-cancelling microphone, and level-dependent function for ambient listening. The headset not only helps protect against hazardous noise, but also makes it easy to communicate in noisy environments and maintain situational awareness.

Supplier: 3M

The Peltor™ WS™ Alert™ XPI Headset is a is high-attenuating hearing protector that can connect up to two Bluetooth® enabled devices, such as a mobile phone and two-way radio. This headset also has a noise-cancelling boom microphone, level-dependent function for ambient listening, push-to-listen feature and built-in FM radio.

Supplier: Biotium

Recognizes a protein of 70 kDa, which is identified as CD86 (HLDA V; WS Code BP BP072. HLDA V; WS Code A A109. HLDA VI; WS Code BP 95. HLDA VI; WS Code B CD86.9). CD86 is a type I transmembrane glycoprotein and a member of the immunoglobulin superfamily of cell surface receptors. It is expressed at high levels on resting peripheral monocytes and dendritic cells and at very low density on resting B and T lymphocytes. CD86 expression is rapidly upregulated by B cell specific stimuli with peak expression at 18 to 42 hours after stimulation. CD86, along with CD80/B71, is an important accessory molecule in T cell co-stimulation via its interaction with CD28 and CD152/CTLA4. Since CD86 has rapid kinetics of induction, it is believed to be the major CD28 ligand expressed early in the immune response. It is also found on malignant Hodgkin and Reed Sternberg (HRS) cells in Hodgkin's disease.

Supplier: Biotium

Recognizes a protein of 70 kDa, which is identified as CD86 (HLDA V; WS Code BP BP072. HLDA V; WS Code A A109. HLDA VI; WS Code BP 95. HLDA VI; WS Code B CD86.9). CD86 is a type I transmembrane glycoprotein and a member of the immunoglobulin superfamily of cell surface receptors. It is expressed at high levels on resting peripheral monocytes and dendritic cells and at very low density on resting B and T lymphocytes. CD86 expression is rapidly upregulated by B cell specific stimuli with peak expression at 18 to 42 hours after stimulation. CD86, along with CD80/B71, is an important accessory molecule in T cell co-stimulation via its interaction with CD28 and CD152/CTLA4. Since CD86 has rapid kinetics of induction, it is believed to be the major CD28 ligand expressed early in the immune response. It is also found on malignant Hodgkin and Reed Sternberg (HRS) cells in Hodgkin's disease.

Supplier: 3M

The 3M™ PELTOR™ WS™ ALERT™ X headset is a Bluetooth® headset with noise-cancelling boom microphone that connects to a mobile phone for hands-free calls and streaming in noisy environments. The headset has a level-dependent function for ambient listening and it synchs to a mobile app for easy set-up and adjustment.

Supplier: Biotium

Recognizes a protein of 70 kDa, which is identified as CD86 (HLDA V; WS Code BP BP072. HLDA V; WS Code A A109. HLDA VI; WS Code BP 95. HLDA VI; WS Code B CD86.9). CD86 is a type I transmembrane glycoprotein and a member of the immunoglobulin superfamily of cell surface receptors. It is expressed at high levels on resting peripheral monocytes and dendritic cells and at very low density on resting B and T lymphocytes. CD86 expression is rapidly upregulated by B cell specific stimuli with peak expression at 18 to 42 hours after stimulation. CD86, along with CD80/B71, is an important accessory molecule in T cell co-stimulation via its interaction with CD28 and CD152/CTLA4. Since CD86 has rapid kinetics of induction, it is believed to be the major CD28 ligand expressed early in the immune response. It is also found on malignant Hodgkin and Reed Sternberg (HRS) cells in Hodgkin's disease.