... , Authors: Dessen P. Published in: Atlas Genet Cytogenet Oncol Haematol.
MDM2 is an E3 ubiquitin ligase that binds and ubiquitinates the tumor suppressor protein p53, leading to its proteasomal degradation. Nutlin-3a (Nutlin) is a preclinical drug that binds MDM2 and prevents the interaction between MDM2 and p53, leading to p53 stabilization and activation of p53 signaling events. Previous studies have reported that Nutlin promotes growth arrest and/or apoptosis in cancer cells that express wild-type p53. In the current study, Nutlin treatment caused a cytoskeletal rearrangement in p53 wild-type human cancer cells from multiple etiologies. Specifically, Nutlin decreased actin stress fibers and reduced the size and number of focal adhesions in treated cells. This process was dependent on p53 expression but was independent of p21 expression and growth arrest. Consistent with this, Nutlin-treated cells failed to form filamentous actin-based motility structures (lamellipodia) and displayed significantly decreased directional persistence in response to migratory cues. ...
Tumor protein p53, encoded in humans by the TP53 gene, was originally identified based on its interaction with the large T antigen of simian virus 40 (SV40). p53 is expressed at low levels in most cell types but is upregulated in many transformed (cancer) cell lines. In response to cellular stress, p53 regulates over 100 target genes that control cell cycle arrest, apoptosis, senescence, DNA repair, and metabolic changes. p53 protein has multiple domains that include DNA-binding, transactivation, and oligomerization activities. Mutations in the TP53 gene cause loss of tumor suppression activity and are found in more than 50% of human tumors. Multiple isoforms of p53 are known, with distinct DNA-binding and transcriptional activation properties. p53 is also known as cellular tumor antigen p53, p53 tumor suppressor, transformation-related protein 53, BCC7, LFS1, TRP53, and antigen NY-CO-13.. ...
Tumor Suppressor Proteins: Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.
Treating Cancer by Tinkering with the Clock E. Cancer is the leading cause of death in North Carolina, and death rates from cancer have been escalating since the early 1980s. One of the most significant advances in cancer prevention and treatment in recent years has been recognition of the importance of apoptosis, or programmed cell death, which provides new opportunities for the discovery of cancer therapeutic targets and agents. The protein tumor suppressor p53 plays a critical role in apoptosis induced by anticancer drugs; however, at least 50 percent of human cancers lack functional p53. Lee discovered that disrupting the circadian clock-the major regulatory system that ensures proper adaptation to the constantly changing environment-functionally activates the p73 tumor suppressor protein, which induces cell death in p53-deficient cancer cells. His study indicates that this mechanism provides another way to overcome the resistance to apoptosis of cancer cells selectively.. ...
Knockout Tested Mouse monoclonal p53 antibody [PAb 1801]. Validated in WB, IP, ELISA, RIA, ChIP and tested in Human. Cited in 44 publication(s). Independently reviewed in 10 review(s).
PIG11 protein may play an important role by interaction with other biological molecules in the regulation of apoptosis and provided us a novel angel of view to explore the possible function of PIG11 in vivo ...
The retinoblastoma and p53 pathways represent the major tumor suppressor pathways in mammals and are crucial for the control of cell proliferation and the response to cellular insults (19-21). Rb is frequently mutated or expressed at low levels in several tumors such as retinoblastoma, osteosarcoma, as well as small lung, prostate, bladder, and breast carcinomas (22-26). Thus, miRNAs controlling Rb protein levels are of high clinical interest. Here, we show that miR-335 efficiently controls Rb1 (pRb/p105) protein levels by directly targeting a conserved region in the 3′UTR of Rb1 in placental mammals. Our data show that miR-335-mediated reduction of Rb1 protein results in the activation of the p53 pathway in human and mouse cells, impairing cell proliferation and neoplastic transformation in vitro. In line with this, impairing the p53 pathway is sufficient to drive hyperproliferation and increased transformation in the context of ectopically increased miR-335 levels. We conclude that miR-335 ...
Evaluation of Coupled Nuclear and Cytoplasmic p53 Dynamics: 10.4018/978-1-4666-3604-0.ch061: The tumor suppressor protein p53 predominantly serves as a sequence specific transcription factor that may be activated upon exposure to diverse stimuli. One
TP53 encodes a major tumor suppressor transcription factor, p53, which plays a significant role in regulating cellular responses to DNA damage and other genomic anomalies.
TP53 encodes a major tumor suppressor transcription factor, p53, which plays a significant role in regulating cellular responses to DNA damage and other genomic anomalies.
Dactinomycin;Tumor Necrosis Factor-alpha;Up-Regulation;Tumor Suppressor Protein p53;Papillomaviridae;Oncogene Proteins, Viral;Ceramides;DNA-Binding Proteins;Repressor Proteins;Cell Cycle Checkpoints;Apoptosis;DNA Damage; ...
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p53 antibody [DO-7] (ready-to-use) (tumor protein p53) for IHC-Fr, IHC-P. Anti-p53 mAb (GTX20911) is tested in Human samples. 100% Ab-Assurance.
Two years ago, OShea discovered that E4-ORF3 clears the way for adenovirus to proliferate by deactivating genes that help the cell defend itself against the virus. "It literally creates zip files of p53 target genes by compressing them until they can no longer be read," she explains. E4-ORF3 self-assembles inside cells into a disordered, web-like structure that captures and inactivates different tumor suppressor protein complexes. Horng Ou, a postdoctoral researcher in OSheas laboratory, says E4-ORF3 is unusual. "It doesnt resemble any known proteins that assemble polymers or that function in cellular tumor suppressor pathways," he says. "Most cellular polymers and filaments form uniform, rigid chains. But E4-ORF3 is the viruss Swiss army knife-it assembles into something that is highly versatile. It has the ability to build itself into all sorts of different shapes and sizes that can capture and deactivate the many defenses of a host cell." In collaboration with scientists from the ...
The tumor suppressor protein p53 is often referred to as the guardian of the genome. In the past, controversial findings have been presented for the role of ...
p73 antibody [N1C1] (tumor protein p73) for ICC/IF, IHC-P, WB. Anti-p73 pAb (GTX109045) is tested in Human samples. 100% Ab-Assurance.
TP63 - TP63 (untagged)-Human tumor protein p63 (TP63), transcript variant 2 available for purchase from OriGene - Your Gene Company.
TP63 - TP63 (untagged)-Human tumor protein p63 (TP63), transcript variant 1 available for purchase from OriGene - Your Gene Company.
Complete information for TP53INP1 gene (Protein Coding), Tumor Protein P53 Inducible Nuclear Protein 1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
Vernon, E. G.; Malik, K.; Reynolds, P.; Powlesland, R.; Dallosso, A. R.; Jackson, S.; Henthorn, K.; Green, E. D.; Brown, K. W. The parathyroid hormone-responsive B1 gene is interrupted by a t(1;7)(q42;p15) breakpoint associated with Wilms tumour. Oncogene 22: 1371-1380, 2003. PubMed ID : (...). ...
Expression of the tumor suppressor p53 is activated in response to cell stress. The dynamics of p53 activation can vary, depending on the stressor, resulting in either pulsatile or constant p53 levels; however, the functional consequence of these different dynamics is unclear. Purvis et al. developed a method to control p53 dynamics in human cells. Pulsing p53 selectively activated genes involved in cell cycle arrest and DNA repair, allowing recovery from DNA damage. In contrast, sustained p53 promoted induction of terminal genes leading to cellular senescence. Thus, protein dynamics can affect cell fate decisions.. J. E. Purvis, K. W. Karhohs, C. Mock, E. Batchelor, A. Loewer, G. Lahav, p53 dynamics control cell fate. Science 336, 1440-1444 (2012). [Abstract] [Full Text] ...
Cytochromes P450 form a very large superfamily of proteins which metabolize substrates from steroids to fatty acids to drugs and are found in organisms from protists to mammals. P450s all appear to take on a similar structural fold, yet frequently having less than 20% sequence identity and having va …
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Effects of exogenous p62-overexpression. (a) H23 cells were transfected with indicated siRNAs for 3 days. After transfection, cell viability was measured, and
p53小鼠单克隆抗体[DO-1](ab1101)可与人样本反应并经WB, IP, ELISA, IHC, Flow Cyt, ChIP, ICC/IF实验严格验证,被8篇文献引用并得到10个独立的用户反馈。
Aileron is the clinical-stage leader in the field of stapled peptide therapeutics for cancers and other diseases. Our lead product candidate ALRN-6924, which is being evaluated in multiple clinical trials, reactivates p53-mediated tumor suppression by targeting both of the primary p53 suppressor proteins, MDMX and MDM2. The p53 protein is long known for its central role in preventing cancer initiation and progression, and its inactivation is essential for the formation of virtually all cancers. We believe that ALRN-6924 is the first and only product candidate in clinical development that can disrupt the interaction of both MDMX and MDM2 to restore p53 function as the bodys first line of defense against cancer.
Aileron is the clinical-stage leader in the field of stapled peptide therapeutics for cancers and other diseases. Our lead product candidate ALRN-6924, which is being evaluated in multiple clinical trials, reactivates p53-mediated tumor suppression by targeting both of the primary p53 suppressor proteins, MDMX and MDM2. The p53 protein is long known for its central role in preventing cancer initiation and progression, and its inactivation is essential for the formation of virtually all cancers. We believe that ALRN-6924 is the first and only product candidate in clinical development that can disrupt the interaction of both MDMX and MDM2 to restore p53 function as the bodys first line of defense against cancer.
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TP53 is the most commonly mutated gene in human cancer for which no effective targeted anti-cancer drug exists. We identified NSC319726 (726) as a mutant p53 re...
Buy anti-TP53BP1 antibody, Mouse anti-Human Tumor Protein p53 Binding Protein 1 (TP53BP1) Monoclonal Antibody-NP_001135451.1 (MBS2090542) product datasheet at MyBioSource, Primary Antibodies. Application: Western Blot (WB), Immunohistochemistry (IHC), Immunocytochemistry (ICC), Immunoprecipitation (IP)
View Notes - Cancer - Copy from BIO 6 at East Los Angeles College. Tumor-suppressor genes help prevent uncontrolled cell growth Tumor-suppressor Proteins: Repair of damaged DNA, control cell adhesion
Tumor protein p53, also known as p53, cellular tumor antigen p53 (UniProt name), phosphoprotein p53, tumor suppressor p53, antigen NY-CO-13, or transformation-related protein 53 (TRP53), is any isoform of a protein encoded by homologous genes in various organisms, such as TP53 (humans) and Trp53 (mice). This homolog (originally thought to be, and often spoken of as, a single protein) is crucial in multicellular organisms, where it prevents cancer formation, thus, functions as a tumor suppressor. As such, p53 has been described as "the guardian of the genome" because of its role in conserving stability by preventing genome mutation. Hence TP53 is classified as a tumor suppressor gene. (Italics are used to denote the TP53 gene name and distinguish it from the protein it encodes.) The name p53 was given in 1979 describing the apparent molecular mass; SDS-PAGE analysis indicates that it is a 53-kilodalton (kDa) protein. However, the actual mass of the full-length p53 protein (p53α) based on the sum ...
The MDM4 gene encodes a nuclear protein that contains a p53 binding domain at the N-terminus and a RING finger domain at the C-terminus. It is the human homolog of mouse double minute 4 (MDM4) protein and shows structural similarity to p53-binding protein MDM2. MDM4 is also called Mdm4 p53 binding protein homolog (mouse); transformed 3T3 cell double minute 4, p53 binding protein (mouse); MDMX, Mdm2-like p53-binding protein, HDMX, MRP1, MDM4-related protein 1, double minute 4 protein, and p53-binding protein Mdm4. Both MDM4 and MDM2 bind the p53 tumor suppressor protein and inhibit its activity, and have been shown to be overexpressed in a variety of human cancers. However, unlike MDM2 which degrades p53, MDM4 inhibits p53 by binding its transcription activation domain. MDM4 can reverse MDM2-targeted degradation of p53, while maintaining suppression of p53 activity.. ...
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p53 Tumor Suppressor Protein Antibody - Without BSA and Azide, Mouse Monoclonal Antibody [Clone DO-7 ] validated in WB, IHC-P, IF, FC (AH10778-100), Abgent
Cellular senescence is an irreversible state of terminal growth arrest that requires functional p53. Acting to block tumor formation, induction of senescence has also been demonstrated to contribute to tumor clearance via the immune system following p53 reactivation.1, 2 The Hdm2-antagonist, Nutlin-3a, has been shown to reactivate p53 and induce a quiescent state in various cancer cell lines,3, 4 similar to the G1 arrest observed upon RNAi targeting of Hdm2 in MCF7 breast cancer.5 In the present study we show that HdmX, a negative regulator of p53, impacts the senescence pathway. Specifically, overexpression of HdmX blocks Ras mediated senescence in primary human fibroblasts. The interaction of HdmX with p53 and the re-localization of HdmX to the nucleus through Hdm2 association appear to be required for this activity. Furthermore, inhibiting HdmX in prostate adenocarcinoma cells expressing wild-type p53, mutant Ras and high levels of HdmX induced cellular senescence as measured by an increase in
This gene encodes a member of the ASPP (apoptosis-stimulating protein of p53) family of p53 interacting proteins. The protein contains four ankyrin repeats and an SH3 domain involved in protein-protein interactions. It is localized to the perinuclear region of the cytoplasm, and regulates apoptosis and cell growth through interactions with other regulatory molecules including members of the p53 family. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008 ...
ATP1B2 Antibody (Center), Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab) validated in WB, IHC-P, FC, E (AP9271c), Abgent
KIAA1644 Antibody (N-term), Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab) validated in IHC-P, WB, E (AP10426a), Abcepta
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Cervical cancer is the second leading cause of death from cancer in women worldwide, and recent epidemiological studies have strongly implicated the sexually transmitted human papillomavirus (HPV) as a causative agent. The ability of high-risk HPVs to contribute to malignant progression seems to depend on expression of the viral E6 and E7 oncogenes. The E6 oncoprotein forms a complex with the cellular tumor suppressor protein p53, leading to degradation of p53 via ubiquitin-dependent proteolysis. Thus, E6 expression results in the loss of p53 function in cells, including stimulation of apoptosis and inhibition of the expression of the antiapoptotic protein bcl-2. Recently, we found increased bcl-2 expression in cervical carcinoma cell lines containing mutated or E6-inactivated p53 (X. L. Liang, S. Mungal, A. Ayscue, J. D. Meissner, P. Wodnicki, G. Gordon, S. Lockett, and B. Herman. J. Cell. Biochem., 57: 509-520, 1995). Based on these findings, we examined Papanicolaou smears from 94 women with ...
Tumor protein p53, a nuclear protein, plays an essential role in the regulation of cell cycle, specifically in the transition from G0 to G1. It is found in very low levels in normal cells, however, in a variety of transformed cell lines, it is expressed in high amounts, and believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing DNA-binding, oligomerization and transcription activation domains. It is postulated to bind as a tetramer to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Alterations of the TP53 gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome ...
Human cancer develops as a result of accumulation of mutations in oncogenes and tumor suppressor genes. Zinc finger protein 668 (ZNF668) has recently been identified and validated as one of the highly mutated genes in breast cancer, but its function is entirely unknown. Here, we report two major functions of ZNF668 in cancer development. (1) ZNF668 functions as a tumor suppressor by regulating p53 protein stability and function. We demonstrate that ZNF668 is a nucleolar protein that physically interacts with both MDM2 and p53. By binding to MDM2, ZNF668 regulates MDM2 autoubiquitination and prevents MDM2-mediated p53 ubiquitination and degradation; ZNF668 deficiency impairs DNA damage-induced p53 stabilization. Notably, ZNF668 effectively suppresses breast cancer cell proliferation and transformation in vitro and tumorigenicity in vivo. Consistently, ZNF668 knockdown readily transforms normal mammary epithelial cells. Together, our studies identify ZNF668 as a novel breast tumor suppressor gene that
The polymorphism SNP309 (rs2279744) in the promoter region of the MDM2 gene has been shown to alter protein expression and may play a role in the susceptibility to lung cancer. The MDM2 protein is a key inhibitor of p53 and several mechanisms of MDM2/p53 interactions are presently known: modulating DNA-repair, cell-cycle control, cell growth and apoptosis. We used 635 Caucasian patients diagnosed with lung cancer before 51 years of age and 1300 healthy gender and age frequency matched population Caucasian controls to investigate the association between the MDM2 SNP309 and the risk of developing early onset lung cancer. Conditional logistic models were applied to assess the genotype-phenotype association, adjusted for smoking. Compared to the GG genotype, the adjusted ORs for the TG and TT genotype were 0.9 (95% CI: 0.7-1.5) and 1.0 ( 95% CI: 0.7-1.5), respectively. Also no association was found for histological subtypes of lung cancer. The strength of this study is that within young cases the ...
Idea Proposed/Formulated by:Dr L Boominathan Ph.D.. Terms & Conditionsapplyhttp://genomediscovery.org/registration/terms-and-conditions/. Citation:Boominathan, Natural product-based therapy for p53-mutated human cancers: Ursolic acid increases the expression of tumor suppressor p53 homologue TAp63 via down regulation of its target gene, 4/March/2015, 8.31 am,Genome-2-Bio-MedicineDiscovery center(GBMD),http://genomediscovery.org. Significance:This study suggests, for the first time, that Ursolic acid,by decreasing the expression of its target gene,it may increase the expression of TAp63. Thereby, it may inhibit cancer progression.Thus,pharmacological formulationsencompassing"Ursolic acid or its analogues" can be used to inhibit the progression of human tumors.. Amount: $ 300*. Undisclosed information:How Ursolic acidincreases the expression ofTAp63. Web:http://genomediscovery.org. Courtesy:When you cite drop us a line [email protected] * Research cooperation. ...