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Description:
The human protooncogene JUN is the putative transforming gene of avian sarcoma virus 17, and it encodes a protein which is highly homologous to the viral protein. cJun (previously known as the Fos binding protein p39) and c Fos form a complex in the nucleus. AP 1 (activating protein 1) is a collective term referring to these dimeric transcription factors composed of Jun, Fos or ATF subunits that bind to a common DNA site, the AP1 binding site. AP 1 proteins, mostly the Jun group, regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21 (cip1/waf1), p19 (ARF) and p16. Fos and Jun proto oncogene expression is induced transiently by a variety of extracellular stimuli associated with mitogenesis, differentiation processes or depolarization of neurons. JUN has been mapped to 1p32 to p31, a chromosomal region involved in both translocations and deletions in human malignancies.
Description:
The human protooncogene JUN is the putative transforming gene of avian sarcoma virus 17, and it encodes a protein which is highly homologous to the viral protein. cJun (previously known as the Fos binding protein p39) and c Fos form a complex in the nucleus. AP 1 (activating protein 1) is a collective term referring to these dimeric transcription factors composed of Jun, Fos or ATF subunits that bind to a common DNA site, the AP1 binding site. AP 1 proteins, mostly the Jun group, regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21 (cip1/waf1), p19 (ARF) and p16. Fos and Jun proto oncogene expression is induced transiently by a variety of extracellular stimuli associated with mitogenesis, differentiation processes or depolarization of neurons. JUN has been mapped to 1p32 to p31, a chromosomal region involved in both translocations and deletions in human malignancies.
Description:
The human protooncogene JUN is the putative transforming gene of avian sarcoma virus 17, and it encodes a protein which is highly homologous to the viral protein. cJun (previously known as the Fos binding protein p39) and c Fos form a complex in the nucleus. AP 1 (activating protein 1) is a collective term referring to these dimeric transcription factors composed of Jun, Fos or ATF subunits that bind to a common DNA site, the AP1 binding site. AP 1 proteins, mostly the Jun group, regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21 (cip1/waf1), p19 (ARF) and p16. Fos and Jun proto oncogene expression is induced transiently by a variety of extracellular stimuli associated with mitogenesis, differentiation processes or depolarization of neurons. JUN has been mapped to 1p32 to p31, a chromosomal region involved in both translocations and deletions in human malignancies.
Description:
Myo-inositol is involved in many important aspects of cellular regulation including membrane structure, signal transduction and osmoregulation. It is taken up into cells by the sodium/myo-inositol cotransporter (SMIT). SMIT activity maintains intracellular concentrations of myo-inositol; it is upregulated in response to hypertonic stress. The human SMIT protein is encoded by the SLC5A3 gene, which maps to chromosome 21q22.12. It is expressed in many human tissues, such as brain, kidney and placenta. Specifically, SMIT is abundantly expressed throughout the whole brain and spinal cord in fetal rat, but is downregulated in adult rat brain with the exception of the choroid plexus, where SMIT expression remains high. In kidney, SMIT localizes to the baso-lateral membranes of the thick ascending limb of Henle (TAL) and the inner medullary collecting duct (IMCD). Impaired SMIT activity is implicated in the pathogenesis of diabetes and Down syndrome.
Description:
Myo-inositol is involved in many important aspects of cellular regulation including membrane structure, signal transduction and osmoregulation. It is taken up into cells by the sodium/myo-inositol cotransporter (SMIT). SMIT activity maintains intracellular concentrations of myo-inositol; it is upregulated in response to hypertonic stress. The human SMIT protein is encoded by the SLC5A3 gene, which maps to chromosome 21q22.12. It is expressed in many human tissues, such as brain, kidney and placenta. Specifically, SMIT is abundantly expressed throughout the whole brain and spinal cord in fetal rat, but is downregulated in adult rat brain with the exception of the choroid plexus, where SMIT expression remains high. In kidney, SMIT localizes to the baso-lateral membranes of the thick ascending limb of Henle (TAL) and the inner medullary collecting duct (IMCD). Impaired SMIT activity is implicated in the pathogenesis of diabetes and Down syndrome.
Description:
Myo-inositol is involved in many important aspects of cellular regulation including membrane structure, signal transduction and osmoregulation. It is taken up into cells by the sodium/myo-inositol cotransporter (SMIT). SMIT activity maintains intracellular concentrations of myo-inositol; it is upregulated in response to hypertonic stress. The human SMIT protein is encoded by the SLC5A3 gene, which maps to chromosome 21q22.12. It is expressed in many human tissues, such as brain, kidney and placenta. Specifically, SMIT is abundantly expressed throughout the whole brain and spinal cord in fetal rat, but is downregulated in adult rat brain with the exception of the choroid plexus, where SMIT expression remains high. In kidney, SMIT localizes to the baso-lateral membranes of the thick ascending limb of Henle (TAL) and the inner medullary collecting duct (IMCD). Impaired SMIT activity is implicated in the pathogenesis of diabetes and Down syndrome.
Description:
The human protooncogene JUN is the putative transforming gene of avian sarcoma virus 17, and it encodes a protein which is highly homologous to the viral protein. cJun (previously known as the Fos binding protein p39) and c Fos form a complex in the nucleus. AP 1 (activating protein 1) is a collective term referring to these dimeric transcription factors composed of Jun, Fos or ATF subunits that bind to a common DNA site, the AP1 binding site. AP 1 proteins, mostly the Jun group, regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21 (cip1/waf1), p19 (ARF) and p16. Fos and Jun proto oncogene expression is induced transiently by a variety of extracellular stimuli associated with mitogenesis, differentiation processes or depolarization of neurons. JUN has been mapped to 1p32 to p31, a chromosomal region involved in both translocations and deletions in human malignancies.
Description:
The human protooncogene JUN is the putative transforming gene of avian sarcoma virus 17, and it encodes a protein which is highly homologous to the viral protein. cJun (previously known as the Fos binding protein p39) and c Fos form a complex in the nucleus. AP 1 (activating protein 1) is a collective term referring to these dimeric transcription factors composed of Jun, Fos or ATF subunits that bind to a common DNA site, the AP1 binding site. AP 1 proteins, mostly the Jun group, regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21 (cip1/waf1), p19 (ARF) and p16. Fos and Jun proto oncogene expression is induced transiently by a variety of extracellular stimuli associated with mitogenesis, differentiation processes or depolarization of neurons. JUN has been mapped to 1p32 to p31, a chromosomal region involved in both translocations and deletions in human malignancies.
Description:
The human protooncogene JUN is the putative transforming gene of avian sarcoma virus 17, and it encodes a protein which is highly homologous to the viral protein. cJun (previously known as the Fos binding protein p39) and c Fos form a complex in the nucleus. AP 1 (activating protein 1) is a collective term referring to these dimeric transcription factors composed of Jun, Fos or ATF subunits that bind to a common DNA site, the AP1 binding site. AP 1 proteins, mostly the Jun group, regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21 (cip1/waf1), p19 (ARF) and p16. Fos and Jun proto oncogene expression is induced transiently by a variety of extracellular stimuli associated with mitogenesis, differentiation processes or depolarization of neurons. JUN has been mapped to 1p32 to p31, a chromosomal region involved in both translocations and deletions in human malignancies.
Description:
The human protooncogene JUN is the putative transforming gene of avian sarcoma virus 17, and it encodes a protein which is highly homologous to the viral protein. cJun (previously known as the Fos binding protein p39) and c Fos form a complex in the nucleus. AP 1 (activating protein 1) is a collective term referring to these dimeric transcription factors composed of Jun, Fos or ATF subunits that bind to a common DNA site, the AP1 binding site. AP 1 proteins, mostly the Jun group, regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21 (cip1/waf1), p19 (ARF) and p16. Fos and Jun proto oncogene expression is induced transiently by a variety of extracellular stimuli associated with mitogenesis, differentiation processes or depolarization of neurons. JUN has been mapped to 1p32 to p31, a chromosomal region involved in both translocations and deletions in human malignancies.
Description:
Bains cylindriques en acier inoxydable avec dispositif de chauffage sous la cuve. Possibilité d'utiliser de l'eau ou de l'huile à faible viscosité (50 cP ou 50 mPa-s) en tant que fluide caloporteur. Le bain dispose d'une plage de vitesse d'agitation de 150 à 800 min<sup>-1</sup> et les dimensions internes du réservoir sont de 200×160 mm (Ø×h).
Description:
Transcription factor required for formation of positional identity in the developing retina, regionalization of the optic chiasm and morphogenesis of the kidney. Can neuralize ectodermal cells directly By similarity. Binds to the consensus sequence 5'-A[AT]T[AG]TTTGTTT-3' and acts as a transcriptional repressor. Also acts as a transcriptional activator. Promotes development of neural crest cells from neural tube progenitors. Restricts neural progenitor cells to the neural crest lineage while suppressing interneuron differentiation. Required for maintenance of pluripotent cells in the pre-implantation and peri-implantation stages of embryogenesis. Probable transcription factor involved in embryogenesis and somatogenesis. FOXD1 is involved in regulating inflammation as well as kidney and retinal development. FOXD1 regulates the activity of NFAT and NFkB. Deficiency of FOXD1 results in multiorgan systemic inflammation, exaggerated Th cell-derived cytokine production, and T cell proliferation in autogolgous MLRs. In kidneys, FOXD1 controls the production of signals required for the normal transition of induced mesenchyme into tubular epithelium and full growth and branching of the collecting system. Deletion of FOXD1 results in renal abnormalities. FOXD2 acts as a modulator of T cell activation.
Description:
Transcription factor required for formation of positional identity in the developing retina, regionalization of the optic chiasm and morphogenesis of the kidney. Can neuralize ectodermal cells directly By similarity. Binds to the consensus sequence 5'-A[AT]T[AG]TTTGTTT-3' and acts as a transcriptional repressor. Also acts as a transcriptional activator. Promotes development of neural crest cells from neural tube progenitors. Restricts neural progenitor cells to the neural crest lineage while suppressing interneuron differentiation. Required for maintenance of pluripotent cells in the pre-implantation and peri-implantation stages of embryogenesis. Probable transcription factor involved in embryogenesis and somatogenesis. FOXD1 is involved in regulating inflammation as well as kidney and retinal development. FOXD1 regulates the activity of NFAT and NFkB. Deficiency of FOXD1 results in multiorgan systemic inflammation, exaggerated Th cell-derived cytokine production, and T cell proliferation in autogolgous MLRs. In kidneys, FOXD1 controls the production of signals required for the normal transition of induced mesenchyme into tubular epithelium and full growth and branching of the collecting system. Deletion of FOXD1 results in renal abnormalities. FOXD2 acts as a modulator of T cell activation.
Description:
Transcription factor required for formation of positional identity in the developing retina, regionalization of the optic chiasm and morphogenesis of the kidney. Can neuralize ectodermal cells directly By similarity. Binds to the consensus sequence 5'-A[AT]T[AG]TTTGTTT-3' and acts as a transcriptional repressor. Also acts as a transcriptional activator. Promotes development of neural crest cells from neural tube progenitors. Restricts neural progenitor cells to the neural crest lineage while suppressing interneuron differentiation. Required for maintenance of pluripotent cells in the pre-implantation and peri-implantation stages of embryogenesis. Probable transcription factor involved in embryogenesis and somatogenesis. FOXD1 is involved in regulating inflammation as well as kidney and retinal development. FOXD1 regulates the activity of NFAT and NFkB. Deficiency of FOXD1 results in multiorgan systemic inflammation, exaggerated Th cell-derived cytokine production, and T cell proliferation in autogolgous MLRs. In kidneys, FOXD1 controls the production of signals required for the normal transition of induced mesenchyme into tubular epithelium and full growth and branching of the collecting system. Deletion of FOXD1 results in renal abnormalities. FOXD2 acts as a modulator of T cell activation.
Description:
The Screen-Well® nephrotoxicity library is a focused collection of 86 compounds with defined and diverse nephrotoxicity, including analgesic nephropathy, interstitial nephritis, glomerularopathy, proximal and distal tubulopathy, acute renal failure, chronic kidney disease, and more. A variety of structurally and mechanistically different compound classes are included, as well as nontoxic controls. Most of the compounds are dissolved in DMSO at 10 mM unless otherwise stated in the documentation provided with the library. Selected compounds are dissolved in DI water. All compounds are provided at 100 μl volumes in a 96-well plate. This library is an essential cost-effective tool for predictive toxicology screening and assay development.
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
Promotion
,BOSSBS-7781R-CY7EA
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