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NDRG1 [MD34R]
Description The N-myc downregulated gene 1 (NDRG1) is a 43 KDa protein that contains a NDRG1 core domain and three unique tandem repeats of 10 hydrophilic amino acids near the COOH terminus, which is ubiquitously expressed in different mammalian tissues and modulates cell growth, differentiation and apoptosis. Although the exact biological function of NDRG1 remains obscure, studies suggest that NDRG1 is a direct transcriptional target gene of p53 to mediated cell death and apoptosis. NDRG1 has been identified as a protein involved in the differentiation of epithelial cells. One of the most well documented links between NDRG1and pathophysiology is its association with inhibition of tumor metastasis. The reduced expression of NDRG1 was found to be associated with tumor metastasis in a variety of tumors, including cancers of the breast, colon, prostate, oral cavity and oropharynx. On the other hand, overexpression of NDRG1 in hepatocellular carcinoma has been an indicator of tumor aggressiveness. Cel Host Rabbit Application Immunocytochemistry (ICC), Immunofluorescence (IF), Immunohistochemistry (IHC), Immunoprecipitation (IP), Western Blot (WB) Reactivity Human, Monkey -
NDRG1 [MD34R]
Description The N-myc downregulated gene 1 (NDRG1) is a 43 KDa protein that contains a NDRG1 core domain and three unique tandem repeats of 10 hydrophilic amino acids near the COOH terminus, which is ubiquitously expressed in different mammalian tissues and modulates cell growth, differentiation and apoptosis. Although the exact biological function of NDRG1 remains obscure, studies suggest that NDRG1 is a direct transcriptional target gene of p53 to mediated cell death and apoptosis. NDRG1 has been identified as a protein involved in the differentiation of epithelial cells. One of the most well documented links between NDRG1and pathophysiology is its association with inhibition of tumor metastasis. The reduced expression of NDRG1 was found to be associated with tumor metastasis in a variety of tumors, including cancers of the breast, colon, prostate, oral cavity and oropharynx. On the other hand, overexpression of NDRG1 in hepatocellular carcinoma has been an indicator of tumor aggressiveness. Cel Host Rabbit Application Immunocytochemistry (ICC), Immunofluorescence (IF), Immunohistochemistry (IHC), Immunoprecipitation (IP), Western Blot (WB) Reactivity Human, Monkey -
NF-κB p65 [MD35R]
Description Transcription factors of the nuclear factor κ B (NF-κB)/Rel family play a pivotal role in inflammatory and immune responses. There are five family members in mammals: RelA, c-Rel, RelB, NF-κB1 (p105/p50), and NF-κB2 (p100/p52). Both p105 and p100 are proteolytically processed by the proteasome to produce p50 and p52, respectively. Rel proteins bind p50 and p52 to form dimeric complexes that bind DNA and regulate transcription. In unstimulated cells, NF-κB is sequestered in the cytoplasm by IκB inhibitory proteins. NF-κB-activating agents can induce the phosphorylation of IκB proteins, targeting them for rapid degradation through the ubiquitin-proteasome pathway and releasing NF-κB to enter the nucleus where it regulates gene expression. NIK and IKKα (IKK1) regulate the phosphorylation and processing of NF-κB2 (p100) to produce p52, which is then translocated to the nucleus. (Shipping Cost: €200.00) Host Rabbit Application Flow cytometry (FC), Chromatin Immunoprecipitation (ChIP), Immunocytochemistry (ICC), Immunofluorescence (IF), Immunohistochemistry (IHC), Western Blot (WB) Reactivity Human, Mouse, Rat, Hamster, Monkey, Dog -
NF-κB p65 [MD35R]
Description Transcription factors of the nuclear factor κ B (NF-κB)/Rel family play a pivotal role in inflammatory and immune responses. There are five family members in mammals: RelA, c-Rel, RelB, NF-κB1 (p105/p50), and NF-κB2 (p100/p52). Both p105 and p100 are proteolytically processed by the proteasome to produce p50 and p52, respectively. Rel proteins bind p50 and p52 to form dimeric complexes that bind DNA and regulate transcription. In unstimulated cells, NF-κB is sequestered in the cytoplasm by IκB inhibitory proteins. NF-κB-activating agents can induce the phosphorylation of IκB proteins, targeting them for rapid degradation through the ubiquitin-proteasome pathway and releasing NF-κB to enter the nucleus where it regulates gene expression. NIK and IKKα (IKK1) regulate the phosphorylation and processing of NF-κB2 (p100) to produce p52, which is then translocated to the nucleus. (Shipping Cost: €200.00) Host Rabbit Application Flow cytometry (FC), Chromatin Immunoprecipitation (ChIP), Immunocytochemistry (ICC), Immunofluorescence (IF), Immunohistochemistry (IHC), Western Blot (WB) Reactivity Human, Mouse, Rat, Hamster, Monkey, Dog -
TRPS1 [EPR16171]
Description Trichorhinophalangeal syndrome I (TRPS1), a transcriptional repressor, binds specifically to GATA sequences and represses expression of GATA-regulated genes at selected sites and stages in vertebrate development. Regulates chondrocyte proliferation and differentiation. Executes multiple functions in proliferating chondrocytes, expanding the region of distal chondrocytes, activating proliferation in columnar cells and supporting the differentiation of columnar into hypertrophic chondrocytes. Defects in TRPS1 are the cause of tricho-rhino-phalangeal syndrome type 1. TRPS1 binds to the NuRD complex via CHD4 and can repress other key transcription factors such as p63 and estrogen receptor. It is expressed at higher levels in androgen-dependent prostate cancers, reducing the expression of PSA. (Shipping Cost: €200.00) Host Rabbit Application Flow cytometry (FC), Immunohistochemistry (IHC), Immunoprecipitation (IP), Western Blot (WB) Reactivity Human, Monkey -
TRPS1 [EPR16171]
Description Trichorhinophalangeal syndrome I (TRPS1), a transcriptional repressor, binds specifically to GATA sequences and represses expression of GATA-regulated genes at selected sites and stages in vertebrate development. Regulates chondrocyte proliferation and differentiation. Executes multiple functions in proliferating chondrocytes, expanding the region of distal chondrocytes, activating proliferation in columnar cells and supporting the differentiation of columnar into hypertrophic chondrocytes. Defects in TRPS1 are the cause of tricho-rhino-phalangeal syndrome type 1. TRPS1 binds to the NuRD complex via CHD4 and can repress other key transcription factors such as p63 and estrogen receptor. It is expressed at higher levels in androgen-dependent prostate cancers, reducing the expression of PSA. (Shipping Cost: €200.00) Host Rabbit Application Flow cytometry (FC), Immunohistochemistry (IHC), Immunoprecipitation (IP), Western Blot (WB) Reactivity Human, Monkey