Proteins & Peptides

p18INK4C is a member of the INK4 family of proteins that regulate the G1 to S cell cycle transition by binding to and inhibiting the pRb kinase activity of cyclin-dependent kinases 4 and 6 (1). Mutation of p18INK4C impairs B-cell terminal differentiation and confers increased susceptibility to tumor development. p18INK4C can function as a tumor suppressor gene in Hodgkins lymphoma and its inactivation may contribute to the cell cycle deregulation and defective terminal differentiation characteristic of the Reed-Sternberg cells (2). p18INK4C Protein is ideal for investigators involved in Signaling Proteins, Cell Cycle Proteins, Cancer, and Cell Cycle research.

p18INK4C is a member of the INK4 family of proteins that regulate the G1 to S cell cycle transition by binding to and inhibiting the pRb kinase activity of cyclin-dependent kinases 4 and 6 (1). Mutation of p18INK4C impairs B-cell terminal differentiation and confers increased susceptibility to tumor development. p18INK4C can function as a tumor suppressor gene in Hodgkins lymphoma and its inactivation may contribute to the cell cycle deregulation and defective terminal differentiation characteristic of the Reed-Sternberg cells (2). p18INK4C Protein is ideal for investigators involved in Signaling Proteins, Cell Cycle Proteins, Cancer, and Cell Cycle research.

p19INK4D protein is associated with CDK6 in several hematopoietic cell lines. It has been demonstrated that p19INK4D expression enhances cell survival under genotoxic conditions (1). By using p19INK4D-overexpressing cells, it has been demonstrated that p19INK4D expression correlates with the cellular resistance to UV treatment with increased DNA repair activity against UV-induced lesions. p19INK4D regulates protein network that integrate DNA repair, apoptosis and checkpoint mechanisms in order to maintain the genomic integrity (2). p19INK4D Protein is ideal for investigators involved in Signaling Proteins, Cell Cycle Proteins, Cancer, and Cell Cycle research.

p19INK4D protein is associated with CDK6 in several hematopoietic cell lines. It has been demonstrated that p19INK4D expression enhances cell survival under genotoxic conditions (1). By using p19INK4D-overexpressing cells, it has been demonstrated that p19INK4D expression correlates with the cellular resistance to UV treatment with increased DNA repair activity against UV-induced lesions. p19INK4D regulates protein network that integrate DNA repair, apoptosis and checkpoint mechanisms in order to maintain the genomic integrity (2). p19INK4D Protein is ideal for investigators involved in Signaling Proteins, Cell Cycle Proteins, Cancer, and Cell Cycle research.

P300 encodes the adenovirus E1A-associated cellular p300 transcriptional co-activator protein (1). P300 is related by sequence to CBP and like CBP can stimulate transcription through activation of CREB. The P300 activity is specifically inhibited by the adenovirus oncoprotein E1A. P300 has also been identified as a co-activator of HIF1A (hypoxia-inducible factor 1 alpha), and thus plays a role in the stimulation of hypoxia-induced genes such as VEGF. P300 is a components of DRAF1 (double-stranded RNA-activated factor-1), a positive regulator of interferon-stimulated gene transcription that functions as a direct response to viral infection (2). P300 Protein is ideal for investigators involved in Signaling Proteins, Acetyl/Methyltransferase Proteins, Apoptosis/Autophagy, Cancer, Cardiovascular Disease, Cell Cycle, ERK/MAPK Pathway, Inflammation, Invasion/Metastasis, Metabolic Disorder, Neurobiology, NfkB Pathway, and PKA/PKC Pathway research.

P300 encodes the adenovirus E1A-associated cellular p300 transcriptional co-activator protein (1). P300 is related by sequence to CBP and like CBP can stimulate transcription through activation of CREB. The P300 activity is specifically inhibited by the adenovirus oncoprotein E1A. P300 has also been identified as a co-activator of HIF1A (hypoxia-inducible factor 1 alpha), and thus plays a role in the stimulation of hypoxia-induced genes such as VEGF. P300 is a components of DRAF1 (double-stranded RNA-activated factor-1), a positive regulator of interferon-stimulated gene transcription that functions as a direct response to viral infection (2). P300 Protein is ideal for investigators involved in Signaling Proteins, Acetyl/Methyltransferase Proteins, Apoptosis/Autophagy, Cancer, Cardiovascular Disease, Cell Cycle, ERK/MAPK Pathway, Inflammation, Invasion/Metastasis, Metabolic Disorder, Neurobiology, NfkB Pathway, and PKA/PKC Pathway research.

p33ING1 displays characteristics of a tumor suppressor protein and can induce cell growth arrest and apoptosis. p33ING1 is a nuclear protein and acute expression of p33 ING1 inhibits cell growth. p33ING1 physically interacts with the tumor suppressor protein TP53 and is a component of the p53 signaling pathway. Mutation of p33ING1 gene occurs in neuroblastoma cells and reduced expression is observed in some breast cancer cell lines (1). It has been proposed that p33ING1 can act as a potent growth regulator in normal and in established cells and plays a role as a candidate tumor suppressor gene whose inactivation may contribute to the development of cancers (2). p33ING1 Protein is ideal for investigators involved in Signaling Proteins, Cell Cycle Proteins, Cancer, and Cell Cycle research.

p33ING1 displays characteristics of a tumor suppressor protein and can induce cell growth arrest and apoptosis. p33ING1 is a nuclear protein and acute expression of p33 ING1 inhibits cell growth. p33ING1 physically interacts with the tumor suppressor protein TP53 and is a component of the p53 signaling pathway. Mutation of p33ING1 gene occurs in neuroblastoma cells and reduced expression is observed in some breast cancer cell lines (1). It has been proposed that p33ING1 can act as a potent growth regulator in normal and in established cells and plays a role as a candidate tumor suppressor gene whose inactivation may contribute to the development of cancers (2). p33ING1 Protein is ideal for investigators involved in Signaling Proteins, Cell Cycle Proteins, Cancer, and Cell Cycle research.

p33ING2 is a member of the inhibitor of growth (ING) family that is associate with and modulates the activity of histone acetyltransferase (HAT) and histone deacetylase (HDAC) complexes and function in DNA repair and apoptosis. P33ING2 is a DNA damage-inducible gene that negatively regulates cell proliferation through activation of p53 by enhancing its acetylation (1). P33ING2 is required for initial DNA damage sensing and chromatin remodeling in the nucleotide excision repair process (2). p33ING2 Protein is ideal for investigators involved in Signaling Proteins, Cell Cycle Proteins, Cancer, and Cell Cycle research.