2649 Results for: "Tween\u00AE+85+(Polisorbat)&pageNo=69"

Supplier: Bioss

Induces susceptibility to atherosclerosis (By similarity). Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. Tyr-69 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes. Prevents phagocyte ingestion of closely apposed viable cells by transmitting 'detachment' signals, and changes function on apoptosis, promoting tethering of dying cells to phagocytes (the encounter of a viable cell with a phagocyte via the homophilic interaction of PECAM1 on both cell surfaces leads to the viable cell's active repulsion from the phagocyte. During apoptosis, the inside-out signaling of PECAM1 is somehow disabled so that the apoptotic cell does not actively reject the phagocyte anymore. The lack of this repulsion signal together with the interaction of the eat-me signals and their respective receptors causes the attachment of the apoptotic cell to the phagocyte, thus triggering the process of engulfment). Isoform Delta15 is unable to protect against apoptosis. Modulates BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in human umbilical cord vein cells (HUVEC).

Supplier: Bioss

Induces susceptibility to atherosclerosis (By similarity). Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. Tyr-69 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes. Prevents phagocyte ingestion of closely apposed viable cells by transmitting 'detachment' signals, and changes function on apoptosis, promoting tethering of dying cells to phagocytes (the encounter of a viable cell with a phagocyte via the homophilic interaction of PECAM1 on both cell surfaces leads to the viable cell's active repulsion from the phagocyte. During apoptosis, the inside-out signaling of PECAM1 is somehow disabled so that the apoptotic cell does not actively reject the phagocyte anymore. The lack of this repulsion signal together with the interaction of the eat-me signals and their respective receptors causes the attachment of the apoptotic cell to the phagocyte, thus triggering the process of engulfment). Isoform Delta15 is unable to protect against apoptosis. Modulates BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in human umbilical cord vein cells (HUVEC).

Supplier: ProSci Inc.

Endothelial Cell Adhesion Molecule (ESAM) is a 55 kDa type I transmembrane glycoprotein member of the JAM family of immunoglobulin superfamily molecules. The 390 amino acid Human ESAM contains a 216 amino acid extracellular domain (ECD) with a V-type and a C2-type immunoglobulin (Ig) domain. ESAM is specifically expressed at endothelial tight junctions and on activated platelets and performs homophilic adhesion activity. The adaptor protein membrane-associated guanylate kinase MAGI-1 has been identified as an intracellular binding partner of ESAM. In addition, ESAM at endothelial tight junctions participates in the migration of neutrophils through the vessel wall, possibly by influencing endothelial cell contacts. ESAM-deficient mice were described with lowered angiogenic potential, and accordingly, overexpression of ESAM is closely associated with certain tumor growth and metastasis. ESAM is expressed on endothelial cells, activated platelets and megakaryocytes. The ECD of human and mouse ESAM share 69% amino acid identity.

Supplier: Bioss

Induces susceptibility to atherosclerosis (By similarity). Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. Tyr-69 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes. Prevents phagocyte ingestion of closely apposed viable cells by transmitting 'detachment' signals, and changes function on apoptosis, promoting tethering of dying cells to phagocytes (the encounter of a viable cell with a phagocyte via the homophilic interaction of PECAM1 on both cell surfaces leads to the viable cell's active repulsion from the phagocyte. During apoptosis, the inside-out signaling of PECAM1 is somehow disabled so that the apoptotic cell does not actively reject the phagocyte anymore. The lack of this repulsion signal together with the interaction of the eat-me signals and their respective receptors causes the attachment of the apoptotic cell to the phagocyte, thus triggering the process of engulfment). Isoform Delta15 is unable to protect against apoptosis. Modulates BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in human umbilical cord vein cells (HUVEC).

Supplier: Bioss

Induces susceptibility to atherosclerosis (By similarity). Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. Tyr-69 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes. Prevents phagocyte ingestion of closely apposed viable cells by transmitting 'detachment' signals, and changes function on apoptosis, promoting tethering of dying cells to phagocytes (the encounter of a viable cell with a phagocyte via the homophilic interaction of PECAM1 on both cell surfaces leads to the viable cell's active repulsion from the phagocyte. During apoptosis, the inside-out signaling of PECAM1 is somehow disabled so that the apoptotic cell does not actively reject the phagocyte anymore. The lack of this repulsion signal together with the interaction of the eat-me signals and their respective receptors causes the attachment of the apoptotic cell to the phagocyte, thus triggering the process of engulfment). Isoform Delta15 is unable to protect against apoptosis. Modulates BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in human umbilical cord vein cells (HUVEC).

Supplier: Bioss

Induces susceptibility to atherosclerosis (By similarity). Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. Tyr-69 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes. Prevents phagocyte ingestion of closely apposed viable cells by transmitting 'detachment' signals, and changes function on apoptosis, promoting tethering of dying cells to phagocytes (the encounter of a viable cell with a phagocyte via the homophilic interaction of PECAM1 on both cell surfaces leads to the viable cell's active repulsion from the phagocyte. During apoptosis, the inside-out signaling of PECAM1 is somehow disabled so that the apoptotic cell does not actively reject the phagocyte anymore. The lack of this repulsion signal together with the interaction of the eat-me signals and their respective receptors causes the attachment of the apoptotic cell to the phagocyte, thus triggering the process of engulfment). Isoform Delta15 is unable to protect against apoptosis. Modulates BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in human umbilical cord vein cells (HUVEC).

Supplier: Bioss

Induces susceptibility to atherosclerosis (By similarity). Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. Tyr-69 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes. Prevents phagocyte ingestion of closely apposed viable cells by transmitting 'detachment' signals, and changes function on apoptosis, promoting tethering of dying cells to phagocytes (the encounter of a viable cell with a phagocyte via the homophilic interaction of PECAM1 on both cell surfaces leads to the viable cell's active repulsion from the phagocyte. During apoptosis, the inside-out signaling of PECAM1 is somehow disabled so that the apoptotic cell does not actively reject the phagocyte anymore. The lack of this repulsion signal together with the interaction of the eat-me signals and their respective receptors causes the attachment of the apoptotic cell to the phagocyte, thus triggering the process of engulfment). Isoform Delta15 is unable to protect against apoptosis. Modulates BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in human umbilical cord vein cells (HUVEC).

Supplier: ProSci Inc.

Endothelial Cell Adhesion Molecule (ESAM) is a 55 kDa type I transmembrane glycoprotein member of the JAM family of immunoglobulin superfamily molecules. The 390 amino acid Human ESAM contains a 216 amino acid extracellular domain (ECD) with a V-type and a C2-type immunoglobulin (Ig) domain. ESAM is specifically expressed at endothelial tight junctions and on activated platelets and performs homophilic adhesion activity. The adaptor protein membrane-associated guanylate kinase MAGI-1 has been identified as an intracellular binding partner of ESAM. In addition, ESAM at endothelial tight junctions participates in the migration of neutrophils through the vessel wall, possibly by influencing endothelial cell contacts. ESAM-deficient mice were described with lowered angiogenic potential, and accordingly, overexpression of ESAM is closely associated with certain tumor growth and metastasis. ESAM is expressed on endothelial cells, activated platelets and megakaryocytes. The ECD of human and mouse ESAM share 69% amino acid identity.

Supplier: ProSci Inc.

Programmed Death-1 (PD-1), firstly cloned from mouse T cell hybridoma 2B4.11, is one member of CD28/CTLA-4 superfamily. PD-1 belongs to type I transmembrane protein and acts as an important immunosuppressive molecule. The cytoplamsic tail of PD-1 contains two structural motifs, an immunoreceptor tyrosine-based inhibitory motif (ITIM) and an immunoreceptor tyrosine-based switch motif (ITSM) formed by two tyrosine residues which make the difference in PD-1 signal mediating. Mouse PD-1 is expressed in thymus and shares about 69% aa sequence identity with human PD-1. Recently, programmed death-1 (PD-1) with its ligands, programmed death ligand B7H1 (PD-L1) and B7DC (PD-L2), was found to regulate T-cell activation and tolerance, upon ligand binding, inhibiting T-cell effector functions in an antigen-specific manner. PD-1 gene knocked out mice would induce some autoimmune diseases, which suggests that PD-1 acts as a co-inhibitory molecule actively participating in maintaining peripheral tolerance. Thus, PD-1 may be a useful target for the immunologic therapy of carcinoma,infection,autoimmune diseases as well as organ transplantation.

Supplier: ProSci Inc.

Programmed Death-1 (PD-1), firstly cloned from mouse T cell hybridoma 2B4.11, is one member of CD28/CTLA-4 superfamily. PD-1 belongs to type I transmembrane protein and acts as an important immunosuppressive molecule. This family also include members of CD28, CTLA-4 and ICOS.The mouse Programmed Death-1 protein, encoded by PD-1 gene, comprises four parts including a putative 20 aa signal peptide, a 149 aa extracellular region, a 21 aa transmembrane domain and a 98 aa cytoplasmic region. The cytoplamsic tail of PD-1 contains two structural motifs, an immunoreceptor tyrosine-based inhibitory motif (ITIM) and an immunoreceptor tyrosine-based switch motif (ITSM) formed by two tyrosine residues which make the difference in PD-1 signal mediating. Mouse PD-1 is expressed in thymus and shares about 69% aa sequence identity with human PD-1. Recently, programmed death-1 (PD-1) with its ligands, programmed death ligand B7H1 (PD-L1) and B7DC (PD-L2), was found to regulate T-cell activation and tolerance, upon ligand binding, inhibiting T-cell effector functions in an antigen-specific manner. PD-1 gene knocked out mice would induce some autoimmune diseases, which suggests that PD-1 acts as a co-inhibitory molecule actively participating in maintaining peripheral tolerance. Thus, PD-1 may be a useful target for the immunologic therapy of carcinoma,infection,autoimmune diseases as well as organ transplantation.

Supplier: Thermo Fisher Scientific

N2,9-Diacetylguanine 99%

Supplier: Thermo Fisher Scientific

Pixantrone maleate

Supplier: Thermo Fisher Scientific

Valganciclovir hydrochloride 97+%

Supplier: Apollo Scientific

4-Ethylbenzotrifluoride 97%

Supplier: Apollo Scientific

2-Methoxy-4-methylbenzonitrile

Supplier: Apollo Scientific

4-Aminopyrimidine-5-carbonitrile

Supplier: Thermo Fisher Scientific

4'-Hydroxynonanophenone 96%

Supplier: Apollo Scientific

5-Fluoroquinoline

Supplier: VWR Chemicals

D-(-)-Ribose ≥98.0%, high purity

Supplier: Apollo Scientific

8-Chloro-1-iodophenazine

Supplier: Thermo Fisher Scientific

EGTA-Na4 (Ethylene glycol bis(2-aminoethyl ether)-N,N,N',N'-tetraacetic acid tetrasodium salt) 95%

Supplier: Apollo Scientific

5-Methylthiophene-2-sulphonamide

Supplier: Apollo Scientific

(4-Chlorooctafluorobutyl)trifluorooxirane

Supplier: Apollo Scientific

2-Fluoro-4-methylbenzenesulphonamide

Supplier: Apollo Scientific

2-Bromo-1-cyclobutylethanone

Supplier: Thermo Fisher Scientific

N-Ethylaniline 98%

Supplier: Apollo Scientific

4-Hydroxy-3-methylbenzaldehyde 99%

Supplier: Apollo Scientific

3-Methyloxolan-3-ol 95%

Supplier: Apollo Scientific

Ethyl 1-isocyanocyclohexanecarboxylate 95%

Supplier: Apollo Scientific

2-(Cyclopropylmethoxy)phenol 95%