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block+heaters+
Numéro de catalogue:
(BOSSBS-3084R-HRP)
Fournisseur:
Bioss
Description:
Key downstream component of the canonical Wnt signaling pathway. In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome. In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes. Involved in the regulation of cell adhesion. Acts as a negative regulator of centrosome cohesion. Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization. Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2. Disrupts PML function and PML-NB formation by inhibiting RANBP2-mediated sumoylation of PML.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3769R-FITC)
Fournisseur:
Bioss
Description:
Modulation of the chromatin structure plays an important role in the regulation of transcription in eukaryotes. The nucleosome, made up of four core histone proteins (H2A, H2B, H3 and H4), is the primary building block of chromatin. The N-terminal tail of core histones undergoes different posttranslational modifications including acetylation, phosphorylation and methylation. These modifications occur in response to cell signal stimuli and have a direct effect on gene expression. In most species, the histone H2B is primarily acetylated at lysines 5, 12, 15 and 20. Histone H3 is primarily acetylated at lysines 9, 14, 18 and 23. Acetylation at lysine 9 appears to have a dominant role in histone deposition and chromatin assembly in some organisms. Phosphorylation at Ser10 of histone H3 is tightly correlated with chromosome condensation during both mitosis and meiosis.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3088R-A555)
Fournisseur:
Bioss
Description:
Key downstream component of the canonical Wnt signaling pathway. In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome. In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes. Involved in the regulation of cell adhesion. Acts as a negative regulator of centrosome cohesion. Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization. Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2. Disrupts PML function and PML-NB formation by inhibiting RANBP2-mediated sumoylation of PML.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-11493R-A647)
Fournisseur:
Bioss
Description:
The UNC5H family of proteins act as transmembrane receptors for netrin-1 and play a crucial role in axon guidance and migration of neural cells. Additionally, UNC5H receptors induce apoptosis when cleaved by a caspase, producing an intracellular fragment containing a death domain. This activity is blocked by the binding of netrin-1. In the absence of netrin-1, UNC5H receptors act as tumor suppressors by inhibiting anchorage-independent growth and invasion, but mutation of these receptors provides a potential mechanism for tumorigenicity. The expression of UNC5H receptors is down-regulated in multiple cancers, including colorectal, breast, ovary, uterus, stomach, lung, and kidney cancers. UNC5H3, also known as UNC5C, plays an important role in the development of spinal accessory motor neurons. It is also involved in mediating the repulsive action for netrin-1 and it serves as a stop signal for migratory cells.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-7781R)
Fournisseur:
Bioss
Description:
Required for S phase entry of the cell cycle.The eukaryotic cell division cycle consists of a number of gene-controlled sequences that involve cyclin dependent kinases (Cdks) and cell division control (Cdc) proteins. Cdc123 (Cell division cycle protein 123), also known as D123, is a 336 amino acid cytoplasmic protein that is involved in cell cycle control. Widely expressed with high expression in thymus, spleen, ovary, testis, small intestine and leukocytes, Cdc123 functions to destabilize Chfr (checkpoint with forkhead and ring finger domain) proteins which, when accumulated, block the G to S phase transition. Cdc123 prevents the Chfr proteins from collecting in the cell, thereby allowing the cell to enter the S phase. Due to its role in cell cycle control, Cdc123 is thought to be a basal marker for luminal breast cancers.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12578R-HRP)
Fournisseur:
Bioss
Description:
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12577R-CY5)
Fournisseur:
Bioss
Description:
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12578R-A488)
Fournisseur:
Bioss
Description:
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12578R-A350)
Fournisseur:
Bioss
Description:
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-9022R-FITC)
Fournisseur:
Bioss
Description:
IQCG is a 443 amino acid protein containing one IQ domain. Widely distributed in nature, the IQ domain forms an amphiphilic seven-turn α-helix capable of binding calmodulin in a Ca2+-independent manner. The level of intracellular calcium is tightly regulated in all eukaryotic cells. A modest increase in this level can result in a myriad of physiological responses, most of which are mediated by calmodulin (CaM), the universal calcium sensor. In acute T-lymphoid/myeloid leukemia, IQCG forms a complex with Nup98, an O-linked glycoprotein and a component of the nuclear pore complex. NUP98-IQCG complex bind co-activators and/or co-repressors, which suggest a role in transcriptional regulation.Nup98-IQCG complex inhibits 32Dcl3 cell apoptosis induced by Arabinofuranosylcytosine (Ara-C) and partially blocks granulocyte differentiation induced by G-CSF. IQCG exists as two isoforms due to alternatively splicing events.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-9022R-A750)
Fournisseur:
Bioss
Description:
IQCG is a 443 amino acid protein containing one IQ domain. Widely distributed in nature, the IQ domain forms an amphiphilic seven-turn -helix capable of binding calmodulin in a Ca2+-independent manner. The level of intracellular calcium is tightly regulated in all eukaryotic cells. A modest increase in this level can result in a myriad of physiological responses, most of which are mediated by calmodulin (CaM), the universal calcium sensor. In acute T-lymphoid/myeloid leukemia, IQCG forms a complex with Nup98, an O-linked glycoprotein and a component of the nuclear pore complex. NUP98-IQCG complex bind co-activators and/or co-repressors, which suggest a role in transcriptional regulation.Nup98-IQCG complex inhibits 32Dcl3 cell apoptosis induced by Arabinofuranosylcytosine (Ara-C) and partially blocks granulocyte differentiation induced by G-CSF. IQCG exists as two isoforms due to alternatively splicing events.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-13508R-FITC)
Fournisseur:
Bioss
Description:
G2A (for G2 accumulation) is a seven transmembrane G protein-coupled receptor that is upregulated in response to DNA damage and stress (1). G2A is predominantly expressed in hematopoietic tissues and in hematopoietic stem cells, and it is more highly detected in pro-B cells, while lower expression is observed in immature B cells and pre-B cells (1,2). G2A is expressed throughout T cell maturation, and it is further increased in response to T-cell activation (3). Ectopic expression of a G2A fusion protein in NIH/3T3 fibroblasts induces a cell cycle arrest that is consistent with a block at the G2/M transition (1,4). G2A is also able to attenuate the proliferative effects of Bcr-Abl, a chimeric tyrosine kinase oncogene, suggesting that G2A possesses anti-oncogenic properties (5). The amino acid sequence of G2A contains a destruction box motif that is consistently observed in cyclins, where it is required for ubiquitination and proteolytic degradation (6).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-13508R-A680)
Fournisseur:
Bioss
Description:
G2A (for G2 accumulation) is a seven transmembrane G protein-coupled receptor that is upregulated in response to DNA damage and stress (1). G2A is predominantly expressed in hematopoietic tissues and in hematopoietic stem cells, and it is more highly detected in pro-B cells, while lower expression is observed in immature B cells and pre-B cells (1,2). G2A is expressed throughout T cell maturation, and it is further increased in response to T-cell activation (3). Ectopic expression of a G2A fusion protein in NIH/3T3 fibroblasts induces a cell cycle arrest that is consistent with a block at the G2/M transition (1,4). G2A is also able to attenuate the proliferative effects of Bcr-Abl, a chimeric tyrosine kinase oncogene, suggesting that G2A possesses anti-oncogenic properties (5). The amino acid sequence of G2A contains a destruction box motif that is consistently observed in cyclins, where it is required for ubiquitination and proteolytic degradation (6).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-13018R-A350)
Fournisseur:
Bioss
Description:
DNA polymerase activity is essential for replication, repair, recombination and mutagenesis. DNA polymerases can often bypass DNA lesions that block DNA replication, thereby allowing the replication of damaged DNA. One such DNA polymerase is the distributive enzyme DNA Pol i, which is encoded by the POLI gene. POLI is located on human chromosome 18q21.2, a region often implicated in the etiology of many human cancers. At thymine templates, DNA Pol i is highly error-prone when replicating undamaged DNA in that it favors the misincorporation of guanine over the correct nucleotide, adenosine. DNA Pol i also promotes the replication of damaged DNA by misincorporating deoxynucleotides opposite DNA lesions. DNA Pol i acts sequentially with DNA Pol Ω, which is essential for damage-induced mutagenesis, to complete the DNA lesion bypass. Therefore, replication involving DNA Pol i is likely to be highly mutagenic.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-13018R-CY3)
Fournisseur:
Bioss
Description:
DNA polymerase activity is essential for replication, repair, recombination and mutagenesis. DNA polymerases can often bypass DNA lesions that block DNA replication, thereby allowing the replication of damaged DNA. One such DNA polymerase is the distributive enzyme DNA Pol i, which is encoded by the POLI gene. POLI is located on human chromosome 18q21.2, a region often implicated in the etiology of many human cancers. At thymine templates, DNA Pol i is highly error-prone when replicating undamaged DNA in that it favors the misincorporation of guanine over the correct nucleotide, adenosine. DNA Pol i also promotes the replication of damaged DNA by misincorporating deoxynucleotides opposite DNA lesions. DNA Pol i acts sequentially with DNA Pol Ω, which is essential for damage-induced mutagenesis, to complete the DNA lesion bypass. Therefore, replication involving DNA Pol i is likely to be highly mutagenic.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-13508R-A647)
Fournisseur:
Bioss
Description:
G2A (for G2 accumulation) is a seven transmembrane G protein-coupled receptor that is upregulated in response to DNA damage and stress (1). G2A is predominantly expressed in hematopoietic tissues and in hematopoietic stem cells, and it is more highly detected in pro-B cells, while lower expression is observed in immature B cells and pre-B cells (1,2). G2A is expressed throughout T cell maturation, and it is further increased in response to T-cell activation (3). Ectopic expression of a G2A fusion protein in NIH/3T3 fibroblasts induces a cell cycle arrest that is consistent with a block at the G2/M transition (1,4). G2A is also able to attenuate the proliferative effects of Bcr-Abl, a chimeric tyrosine kinase oncogene, suggesting that G2A possesses anti-oncogenic properties (5). The amino acid sequence of G2A contains a destruction box motif that is consistently observed in cyclins, where it is required for ubiquitination and proteolytic degradation (6).
UOM:
1 * 100 µl
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