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Código de Artigo: (BOSSBS-4286R-A555)
Fornecedor: Bioss
Descrição: Exchange factor for GTP-binding proteins RhoA, RhoG and, to a lesser extent, Rac1. Binds physically to the nucleotide-free states of those GTPases (By similarity). Plays an important role in angiogenesis. Its recruitment by phosphorylated EPHA2 is critical for EFNA1-induced RAC1 GTPase activation and vascular endothelial cell migration and assembly. May be important for integrin-mediated signaling, at least in some cell types. In osteoclasts, along with SYK tyrosine kinase, required for signaling through integrin alpha-v/beta-1 (ITAGV-ITGB1), a crucial event for osteoclast proper cytoskeleton organization and function. This signaling pathway involves RAC1, but not RHO, activation. Necessary for proper wound healing. In the course of wound healing, required for the phagocytotic cup formation preceding macrophage phagocytosis of apoptotic neutrophils. Responsible for integrin beta-2-mediated macrophage adhesion and, to a lesser extent, contributes to beta-3-mediated adhesion. Does not affect integrin beta-1-mediated adhesion.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-13662R)
Fornecedor: Bioss
Descrição: The translational product of the Vav proto-oncogene is exclusively expressed in cells of hematopoietic origin and is critical for lymphocyte development and activation. However, the biochemical basis of Vav’s function is unclear. Vav contains a single SH2 domain that is required for its association with the T cell receptor (TCR). Overexpression of Vav or SLP-76 in Jurkat cells leads to NFAT activation and IL-2 production. When co-expressed, Vav and SLP-76 synergize to induce a robust basal and TCR-mediated IL-2 response. Although SLP-76 does not contain a motif that would indicate it to be a member of the tyrosine, serine/threonine or lipid kinase families, it does contain several putative SH2/SH3-binding domains and has been shown to physically associate with the adapter protein GRB2 as well as PLC g1. The discovery of SLP-76 represents an important step in elucidating the mechanism of Vav transformation and TCR-mediated NFAT activation.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-4286R-HRP)
Fornecedor: Bioss
Descrição: Exchange factor for GTP-binding proteins RhoA, RhoG and, to a lesser extent, Rac1. Binds physically to the nucleotide-free states of those GTPases (By similarity). Plays an important role in angiogenesis. Its recruitment by phosphorylated EPHA2 is critical for EFNA1-induced RAC1 GTPase activation and vascular endothelial cell migration and assembly. May be important for integrin-mediated signaling, at least in some cell types. In osteoclasts, along with SYK tyrosine kinase, required for signaling through integrin alpha-v/beta-1 (ITAGV-ITGB1), a crucial event for osteoclast proper cytoskeleton organization and function. This signaling pathway involves RAC1, but not RHO, activation. Necessary for proper wound healing. In the course of wound healing, required for the phagocytotic cup formation preceding macrophage phagocytosis of apoptotic neutrophils. Responsible for integrin beta-2-mediated macrophage adhesion and, to a lesser extent, contributes to beta-3-mediated adhesion. Does not affect integrin beta-1-mediated adhesion.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-4286R-CY7)
Fornecedor: Bioss
Descrição: Exchange factor for GTP-binding proteins RhoA, RhoG and, to a lesser extent, Rac1. Binds physically to the nucleotide-free states of those GTPases (By similarity). Plays an important role in angiogenesis. Its recruitment by phosphorylated EPHA2 is critical for EFNA1-induced RAC1 GTPase activation and vascular endothelial cell migration and assembly. May be important for integrin-mediated signaling, at least in some cell types. In osteoclasts, along with SYK tyrosine kinase, required for signaling through integrin alpha-v/beta-1 (ITAGV-ITGB1), a crucial event for osteoclast proper cytoskeleton organization and function. This signaling pathway involves RAC1, but not RHO, activation. Necessary for proper wound healing. In the course of wound healing, required for the phagocytotic cup formation preceding macrophage phagocytosis of apoptotic neutrophils. Responsible for integrin beta-2-mediated macrophage adhesion and, to a lesser extent, contributes to beta-3-mediated adhesion. Does not affect integrin beta-1-mediated adhesion.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-13663R)
Fornecedor: Bioss
Descrição: The translational product of the Vav proto-oncogene is exclusively expressed in cells of hematopoietic origin and is critical for lymphocyte development and activation. However, the biochemical basis of Vav’s function is unclear. Vav contains a single SH2 domain that is required for its association with the T cell receptor (TCR). Overexpression of Vav or SLP-76 in Jurkat cells leads to NFAT activation and IL-2 production. When co-expressed, Vav and SLP-76 synergize to induce a robust basal and TCR-mediated IL-2 response. Although SLP-76 does not contain a motif that would indicate it to be a member of the tyrosine, serine/threonine or lipid kinase families, it does contain several putative SH2/SH3-binding domains and has been shown to physically associate with the adapter protein GRB2 as well as PLC g1. The discovery of SLP-76 represents an important step in elucidating the mechanism of Vav transformation and TCR-mediated NFAT activation.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-0615R-CY5.5)
Fornecedor: Bioss
Descrição: Multitasking protein that has dual roles in promoting cell proliferation and preventing apoptosis. Component of a chromosome passage protein complex (CPC) which is essential for chromosome alignment and segregation during mitosis and cytokinesis. Acts as an important regulator of the localization of this complex; directs CPC movement to different locations from the inner centromere during prometaphase to midbody during cytokinesis and participates in the organization of the center spindle by associating with polymerized microtubules. The complex with RAN plays a role in mitotic spindle formation by serving as a physical scaffold to help deliver the RAN effector molecule TPX2 to microtubules. May counteract a default induction of apoptosis in G2/M phase. The acetylated form represses STAT3 transactivation of target gene promoters. May play a role in neoplasia. Inhibitor of CASP3 and CASP7. Isoform 2 and isoform 3 do not appear to play vital roles in mitosis. Isoform 3 shows a marked reduction in its anti-apoptotic effects when compared with the displayed wild-type isoform.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-4286R-CY5)
Fornecedor: Bioss
Descrição: Exchange factor for GTP-binding proteins RhoA, RhoG and, to a lesser extent, Rac1. Binds physically to the nucleotide-free states of those GTPases (By similarity). Plays an important role in angiogenesis. Its recruitment by phosphorylated EPHA2 is critical for EFNA1-induced RAC1 GTPase activation and vascular endothelial cell migration and assembly. May be important for integrin-mediated signaling, at least in some cell types. In osteoclasts, along with SYK tyrosine kinase, required for signaling through integrin alpha-v/beta-1 (ITAGV-ITGB1), a crucial event for osteoclast proper cytoskeleton organization and function. This signaling pathway involves RAC1, but not RHO, activation. Necessary for proper wound healing. In the course of wound healing, required for the phagocytotic cup formation preceding macrophage phagocytosis of apoptotic neutrophils. Responsible for integrin beta-2-mediated macrophage adhesion and, to a lesser extent, contributes to beta-3-mediated adhesion. Does not affect integrin beta-1-mediated adhesion.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-4286R-A350)
Fornecedor: Bioss
Descrição: Exchange factor for GTP-binding proteins RhoA, RhoG and, to a lesser extent, Rac1. Binds physically to the nucleotide-free states of those GTPases (By similarity). Plays an important role in angiogenesis. Its recruitment by phosphorylated EPHA2 is critical for EFNA1-induced RAC1 GTPase activation and vascular endothelial cell migration and assembly. May be important for integrin-mediated signaling, at least in some cell types. In osteoclasts, along with SYK tyrosine kinase, required for signaling through integrin alpha-v/beta-1 (ITAGV-ITGB1), a crucial event for osteoclast proper cytoskeleton organization and function. This signaling pathway involves RAC1, but not RHO, activation. Necessary for proper wound healing. In the course of wound healing, required for the phagocytotic cup formation preceding macrophage phagocytosis of apoptotic neutrophils. Responsible for integrin beta-2-mediated macrophage adhesion and, to a lesser extent, contributes to beta-3-mediated adhesion. Does not affect integrin beta-1-mediated adhesion.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-8257R-CY7)
Fornecedor: Bioss
Descrição: Probable transcriptional regulator involved in developmental processes. Is required for normal development of the pharyngeal arch arteries.Involvement in disease:Haploinsufficiency of the TBX1 gene is responsible for most of the physical malformations present in DiGeorge syndrome (DGS) and velocardiofacial syndrome (VCFS) . DGS is characterized by the association of several malformations: hypoplastic thymus and parathyroid glands, congenital conotruncal cardiopathy, and a subtle but characteristic facial dysmorphology. VCFS is marked by the association of congenital conotruncal heart defects, cleft palate or velar insufficiency, facial dysmorpholgy and learning difficulties. It is now accepted that these two syndromes represent two forms of clinical expression of the same entity manifesting at different stages of life.Defects in TBX1 are a cause of DiGeorge syndrome (DGS) .Defects in TBX1 are a cause of velocardiofacial syndrome (VCFS) .Defects in TBX1 are a cause of conotruncal heart malformations (CTHM). CTHM consist of cardiac outflow tract defects, such as tetralogy of Fallot, pulmonary atresia, double-outlet right ventricle, truncus arteriosus communis, and aortic arch anomalies.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-13661R-HRP)
Fornecedor: Bioss
Descrição: The translational product of the Vav proto-oncogene is exclusively expressed in cells of hematopoietic origin and is critical for lymphocyte development and activation. However, the biochemical basis of Vav’s function is unclear. Vav contains a single SH2 domain that is required for its association with the T cell receptor (TCR). Overexpression of Vav or SLP-76 in Jurkat cells leads to NFAT activation and IL-2 production. When co-expressed, Vav and SLP-76 synergize to induce a robust basal and TCR-mediated IL-2 response. Although SLP-76 does not contain a motif that would indicate it to be a member of the tyrosine, serine/threonine or lipid kinase families, it does contain several putative SH2/SH3-binding domains and has been shown to physically associate with the adapter protein GRB2 as well as PLC g1. The discovery of SLP-76 represents an important step in elucidating the mechanism of Vav transformation and TCR-mediated NFAT activation.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-8257R-CY3)
Fornecedor: Bioss
Descrição: Probable transcriptional regulator involved in developmental processes. Is required for normal development of the pharyngeal arch arteries.Involvement in disease:Haploinsufficiency of the TBX1 gene is responsible for most of the physical malformations present in DiGeorge syndrome (DGS) and velocardiofacial syndrome (VCFS) . DGS is characterized by the association of several malformations: hypoplastic thymus and parathyroid glands, congenital conotruncal cardiopathy, and a subtle but characteristic facial dysmorphology. VCFS is marked by the association of congenital conotruncal heart defects, cleft palate or velar insufficiency, facial dysmorpholgy and learning difficulties. It is now accepted that these two syndromes represent two forms of clinical expression of the same entity manifesting at different stages of life.Defects in TBX1 are a cause of DiGeorge syndrome (DGS) .Defects in TBX1 are a cause of velocardiofacial syndrome (VCFS) .Defects in TBX1 are a cause of conotruncal heart malformations (CTHM). CTHM consist of cardiac outflow tract defects, such as tetralogy of Fallot, pulmonary atresia, double-outlet right ventricle, truncus arteriosus communis, and aortic arch anomalies.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-8257R-A750)
Fornecedor: Bioss
Descrição: Probable transcriptional regulator involved in developmental processes. Is required for normal development of the pharyngeal arch arteries.Involvement in disease:Haploinsufficiency of the TBX1 gene is responsible for most of the physical malformations present in DiGeorge syndrome (DGS) and velocardiofacial syndrome (VCFS) . DGS is characterised by the association of several malformations: hypoplastic thymus and parathyroid glands, congenital conotruncal cardiopathy, and a subtle but characteristic facial dysmorphology. VCFS is marked by the association of congenital conotruncal heart defects, cleft palate or velar insufficiency, facial dysmorpholgy and learning difficulties. It is now accepted that these two syndromes represent two forms of clinical expression of the same entity manifesting at different stages of life.Defects in TBX1 are a cause of DiGeorge syndrome (DGS) .Defects in TBX1 are a cause of velocardiofacial syndrome (VCFS) .Defects in TBX1 are a cause of conotruncal heart malformations (CTHM). CTHM consist of cardiac outflow tract defects, such as tetralogy of Fallot, pulmonary atresia, double-outlet right ventricle, truncus arteriosus communis, and aortic arch anomalies.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-8257R-FITC)
Fornecedor: Bioss
Descrição: Probable transcriptional regulator involved in developmental processes. Is required for normal development of the pharyngeal arch arteries.Involvement in disease:Haploinsufficiency of the TBX1 gene is responsible for most of the physical malformations present in DiGeorge syndrome (DGS) and velocardiofacial syndrome (VCFS) . DGS is characterized by the association of several malformations: hypoplastic thymus and parathyroid glands, congenital conotruncal cardiopathy, and a subtle but characteristic facial dysmorphology. VCFS is marked by the association of congenital conotruncal heart defects, cleft palate or velar insufficiency, facial dysmorpholgy and learning difficulties. It is now accepted that these two syndromes represent two forms of clinical expression of the same entity manifesting at different stages of life.Defects in TBX1 are a cause of DiGeorge syndrome (DGS) .Defects in TBX1 are a cause of velocardiofacial syndrome (VCFS) .Defects in TBX1 are a cause of conotruncal heart malformations (CTHM). CTHM consist of cardiac outflow tract defects, such as tetralogy of Fallot, pulmonary atresia, double-outlet right ventricle, truncus arteriosus communis, and aortic arch anomalies.
UOM: 1 * 100 µl


Código de Artigo: (BOSSBS-0615R-FITC)
Fornecedor: Bioss
Descrição: Multitasking protein that has dual roles in promoting cell proliferation and preventing apoptosis. Component of a chromosome passage protein complex (CPC) which is essential for chromosome alignment and segregation during mitosis and cytokinesis. Acts as an important regulator of the localization of this complex; directs CPC movement to different locations from the inner centromere during prometaphase to midbody during cytokinesis and participates in the organization of the center spindle by associating with polymerized microtubules. The complex with RAN plays a role in mitotic spindle formation by serving as a physical scaffold to help deliver the RAN effector molecule TPX2 to microtubules. May counteract a default induction of apoptosis in G2/M phase. The acetylated form represses STAT3 transactivation of target gene promoters. May play a role in neoplasia. Inhibitor of CASP3 and CASP7. Isoform 2 and isoform 3 do not appear to play vital roles in mitosis. Isoform 3 shows a marked reduction in its anti-apoptotic effects when compared with the displayed wild-type isoform.
UOM: 1 * 100 µl


Código de Artigo: (ENZOADI905798100)
Fornecedor: ENZO LIFE SCIENCES
Descrição: Neuropeptide Y (NPY) and the closely related peptide YY (PYY) and pancreatic polypeptide (PP) are a family of 36-amino acid, tyrosine-rich peptides with amidated C-terminal ends that are known to regulate gastrointestinal and central nervous system functions including food intake and the inhibition of anxiety. Four functional NPY receptors (Y1/Y2/Y4/Y5) have been identified to date, with a fifth (y6) being a non-functional receptor in primates that is absent from the rat genome. Y1, Y2, and Y5 receptors preferentially bind NPY and PYY, while the Y4 receptor preferentially binds PP. All four receptors signal via coupling to Gi/o alpha subunits, inhibiting adenylyl cyclase activity, thereby decreasing intracellular cAMP levels. Y1 receptor deficient mice display a variety of physical and behavioral phenotypes including obesity, hyperinsulinemia, and increased territorial behavior.
UOM: 1 * 100 µG


Código de Artigo: (BOSSBS-8257R-HRP)
Fornecedor: Bioss
Descrição: Probable transcriptional regulator involved in developmental processes. Is required for normal development of the pharyngeal arch arteries.Involvement in disease:Haploinsufficiency of the TBX1 gene is responsible for most of the physical malformations present in DiGeorge syndrome (DGS) and velocardiofacial syndrome (VCFS) . DGS is characterized by the association of several malformations: hypoplastic thymus and parathyroid glands, congenital conotruncal cardiopathy, and a subtle but characteristic facial dysmorphology. VCFS is marked by the association of congenital conotruncal heart defects, cleft palate or velar insufficiency, facial dysmorpholgy and learning difficulties. It is now accepted that these two syndromes represent two forms of clinical expression of the same entity manifesting at different stages of life.Defects in TBX1 are a cause of DiGeorge syndrome (DGS) .Defects in TBX1 are a cause of velocardiofacial syndrome (VCFS) .Defects in TBX1 are a cause of conotruncal heart malformations (CTHM). CTHM consist of cardiac outflow tract defects, such as tetralogy of Fallot, pulmonary atresia, double-outlet right ventricle, truncus arteriosus communis, and aortic arch anomalies.
UOM: 1 * 100 µl


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O stock para este item é limitado. Por favor, certifique-se de que efetuou o seu login para visualizar o stock disponível. Se a call está visível e precisar de ajuda, por favor, ligue para 213 600 770
Este produto é sujeito a regulamentação especifica.
Em caso de encomenda, será contactado a solicitar documentação complementar necessária e/ou obrigatória (licença, autorização ou declaração de uso final) para a continuidade do pedido. Agradecemos a vossa compreensão
Este produto é sujeito a regulamentação especifica.
Em caso de encomenda, será contactado a solicitar documentação complementar necessária e/ou obrigatória (licença, autorização ou declaração de uso final) para a continuidade do pedido. Agradecemos a vossa compreensão.
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