• p53 can activate a variety of signaling pathways to inhibit tumors, such as cell cycle arrest, cell senescence, apoptosis or iron death. (medicaltrend.org)
  • p53 plays a role in regulation or progression through the cell cycle, apoptosis, and genomic stability by means of several mechanisms: It can activate DNA repair proteins when DNA has sustained damage. (wikipedia.org)
  • Conclusion: For the protection of stem cells against apoptosis, different pathways, namely Phosphoinositide 3-Kinase (PI3K/AKT), Hypoxia-Inducible Factor (HIF1), Mitogen-Activated Protein Kinases (MAPK) and Hippo, are discussed. (benthamscience.com)
  • Reactivation of p53 in established tumors typically results in one of two cell fates, cell cycle arrest or apoptosis, but it remains unclear how this cell fate is determined. (nih.gov)
  • We hypothesized that high mitochondrial priming prior to p53 reactivation would lead to apoptosis, while low priming would lead to survival and cell cycle arrest. (nih.gov)
  • Using a panel of Kras-driven, p53 restorable cell lines derived from genetically engineered mouse models of lung adenocarcinoma and sarcoma (both of which undergo cell cycle arrest upon p53 restoration), as well as lymphoma (which instead undergo apoptosis), we show that the level of mitochondrial apoptotic priming is a critical determinant of p53 reactivation outcome. (nih.gov)
  • Cells with high initial priming (e.g., lymphomas) lacked sufficient reserve antiapoptotic capacity and underwent apoptosis after p53 restoration. (nih.gov)
  • When primed by inhibition of their antiapoptotic proteins using genetic (BCL-2 or BCL-XL deletion or BAD overexpression) or pharmacologic (navitoclax) means, apoptosis resulted upon p53 restoration in vitro and in vivo. (nih.gov)
  • The p53 protein is an important tumor suppressor that is essential for regulating cell division, senescence, and self-destruction (apoptosis). (medlineplus.gov)
  • p53 mediates cell cycle arrest or apoptosis in response to DNA damage or starvation for pyrimidine nucleotides. (thermofisher.com)
  • In other situations the response is cell cycle arrest or programmed cell death (apoptosis), providing a barrier to further tumour development that the tumour may ultimately circumvent through the acquisition of a mutation in one of the genes within the stress-response pathway. (southampton.ac.uk)
  • Fosfoproteína nuclear codificada por el gen p53 (GENES P53) cuya función normal es controlar la PROLIFERACIÓN CELULAR y la APOPTOSIS. (bvsalud.org)
  • Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. (bvsalud.org)
  • p53 is a transcription factor that participates in cell cycle checkpoint processes and apoptosis. (lu.se)
  • p53 is one of the most important tumor suppressor genes, and more than half of cancer patients carry mutations in the p53 gene. (medicaltrend.org)
  • What is interesting is that although these mice showed activation of p53 (for example, the up-regulation of p53 target genes was observed in different tissues), the content of p53 protein did not increase significantly. (medicaltrend.org)
  • Global CpG island hypermethylation, which induces epigenetic silencing of tumor suppressor genes, is also a unique feature of EBVaGC and is considered to be crucial for its carcinogenesis. (spandidos-publications.com)
  • p53 is up-regulated in response to stress signals and stimulated to activate transcription of specific genes, resulting in expression of p21waf1 and other proteins involved in G1 or G2/M arrest. (thermofisher.com)
  • p53, also known as Tumor protein P53, cellular tumor antigen p53 (UniProt name), or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. (wikipedia.org)
  • Studies of human embryonic stem cells (hESCs) commonly describe the nonfunctional p53-p21 axis of the G1/S checkpoint pathway with subsequent relevance for cell cycle regulation and the DNA damage response (DDR). (wikipedia.org)
  • Our study additionally shows that the majority of AT heterozygotes express almost halved levels of ATM protein, sufficient in most cases to normally regulate the ATM-dependent DNA damage-response pathway. (nih.gov)
  • In order to escape the safeguard system mediated by p53, nearly all human cancers have compromised the effectiveness of the p53 pathway. (europa.eu)
  • Along the same lines, p53 is mostly degraded following the ubiquitin/proteasome pathway and calpains also seem to participate in its degradation. (cnrs.fr)
  • SRSF2 Regulation of MDM2 Reveals Splicing as a Therapeutic Vulnerability of the p53 Pathway. (umassmed.edu)
  • In some circumstances, the activation of a stress-response pathway will actually help the tumour cell to survive and proliferate. (southampton.ac.uk)
  • The p53 tumour suppressor protein is a key component of one such stress-response pathway, and virtually all cancers loose functionality of the p53-stress response pathway. (southampton.ac.uk)
  • In the late 1990s work from a number of groups, including Blaydes et al , demonstrated that HDM2 could be targeted in cancer cells to re-activate the p53 stress-response pathway. (southampton.ac.uk)
  • In response to DNA-damaging agents, the wild-type p53-activated fragment 1 (WAF1 also known as p21) is an important downstream effector in the p53-specific growth arrest pathway. (lu.se)
  • The UPS and UBL proteins studied by us are: the oncogenic E3 ligase Mdm2, which regulates levels of p53, the deubiquitinating enzyme (DUB) USP2a, and the UBL protein Hub1, which has been recently shown to control alternative splicing by non-covalent binding to the Snu66 spliceosomal protein. (europa.eu)
  • Human papillomavirus oncogenic E6 protein regulates human β-defensin 3 (hBD3) expression via the tumor suppressor protein p53. (antikoerper-online.de)
  • Phosphorylation of the Mdm2 oncoprotein by the c-Abl tyrosine kinase regulates p53 tumor suppression and the radiosensitivity of mice. (umassmed.edu)
  • The CBP (CREB-binding protein) is a histone acetyltransferase and transcriptional coactivator that regulates RNA polymerase II transcription. (novusbio.com)
  • As such, p53 has been described as "the guardian of the genome" because of its role in conserving stability by preventing genome mutation. (wikipedia.org)
  • The tumour suppressor p53 protein, ""the guardian of the genome"", has an overarching role in protecting the organism from cancer. (europa.eu)
  • To investigate the involvement of HPV 16/18 E6 in p53 inactivation in pterygium, the association between HPV 16 or HPV 18 infection, the HPV E6 oncoprotein, and p53 protein expression was analyzed in this study. (molvis.org)
  • In addition, p53 protein negative expression in pterygium was correlated with HPV16/18 E6 oncoprotein expression but not with a p53 mutation. (molvis.org)
  • In this report, we analyzed p53 protein expression and gene mutation in pterygium in comparison with HPV 16/18 infection and E6 oncoprotein expression in pterygium tissues to understand whether the HPV infection was involved in pterygium pathogenesis. (molvis.org)
  • Some Example Projects: Regulation of HDM2 and HDMX proteins The HDM2 oncoprotein is the major negative regulator of p53 function in the cell. (southampton.ac.uk)
  • Role of CtBP transcriptional repressors in cancer cell proliferation and survival In common with p53, CtBP1 and CtBP2 proteins were discovered through their physical association with a viral oncoprotein. (southampton.ac.uk)
  • This is mainly because there are many proteins that regulate p53 levels in cells, the most important of which is MDM2. (medicaltrend.org)
  • We have shown that CtBPs also interact with HDM2 protein, and can consequently regulate p53 function (Mirnezami et al, 2003). (southampton.ac.uk)
  • Thus, altering the apo structure of p53 changed its DNA binding properties, even though the DNA-bound structure was not altered. (rcsb.org)
  • The structure of p53 comprises an N-terminal transactivation domain, a central DNA-binding domain, an oligomerisation domain, and a C-terminal regulatory domain. (thermofisher.com)
  • This 6KQ mutation firstly makes p53 no longer be ubiquitinated by MDM2, and secondly it can also release its binding to certain transcriptional repressors. (medicaltrend.org)
  • HPV 16/18 infection was detected by nested-polymerase chain reaction (nested-PCR), the p53 mutation was detected by direct sequencing, and the p53 and the HPV 16/18 E6 proteins were studied using immunohistochemistry on 129 pterygial specimens and 20 normal conjunctivas. (molvis.org)
  • Double-strand break (DSB) repair protein involved in response to DNA damage, telomere dynamics and class-switch recombination (CSR) during antibody genesis. (cusabio.com)
  • p53 was recognized by immunoblotting by using an anti-p53 antibody. (cancer-pictures.org)
  • The following product was used in this experiment: P53 Monoclonal Antibody (5B10) from Thermo Fisher Scientific, catalog # BSM-33209M. (thermofisher.com)
  • The tumor suppressor protein, p53, is a sequence specific transcription factor that is activated by cellular stress. (thermofisher.com)
  • Autophagy is a cellular catabolic process that eliminates damaged cell organelles, unfolded proteins, and various intracellular pathogens through lysosomal degradation. (hindawi.com)
  • After the degradation of damaged proteins and lipids, amino acids and fatty acids are released into the cytoplasm and recycled for new biosynthesis of cellular components or energy production [ 4 ]. (hindawi.com)
  • Host Response to Tumors The immune response to foreign antigens consists of Humoral mechanisms (eg, antibodies) Cellular mechanisms (See also Tumor Antigens. (msdmanuals.com)
  • Similarly, for p53 to function as a tumor suppressor gene, it also needs to get rid of MDM2-mediated degradation, so as to stabilize the p53 protein to function. (medicaltrend.org)
  • Are there multiple proteolytic pathways contributing to c-Fos, c-Jun and p53 protein degradation in vivo? (cnrs.fr)
  • In general, autophagy degrades long-lived damaged intracellular proteins, in contrast to the ubiquitin-proteasome system, which controls the degradation of short-lived proteins [ 2 ]. (hindawi.com)
  • The traditional theory is that when cells are stimulated, the binding of MDM2 and p53 will be destroyed, leading to the accumulation of p53 protein, which affects downstream gene expression and enables cells to respond to the stimulus. (medicaltrend.org)
  • MDM2 ubiquitination of p53 mainly occurs on the six Ks (K369, K370, K378, K379, K383, and K384) of the C-terminal domain of p53. (medicaltrend.org)
  • The restoration of the impaired function of the single gene, p53, by disrupting the Mdm2- p53/Mdmx-p53 interactions, offers a fundamentally new avenue for anticancer therapy across a broad spectrum of cancers. (europa.eu)
  • Proto-Oncogene Proteins c-mdm2" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • This graph shows the total number of publications written about "Proto-Oncogene Proteins c-mdm2" by people in this website by year, and whether "Proto-Oncogene Proteins c-mdm2" was a major or minor topic of these publications. (umassmed.edu)
  • Below are the most recent publications written about "Proto-Oncogene Proteins c-mdm2" by people in Profiles. (umassmed.edu)
  • TP53 gene encodes proteins that bind to DNA and regulate gene expression to prevent mutations of the genome. (wikipedia.org)
  • On Western blots, the full-length ATM protein was detected in eight of 18 AT cases, albeit at 1-32% of the normal levels, whereas a truncated ATM protein was detected in a single case, despite the prevalence among cases of truncation mutations. (nih.gov)
  • Altogether, our study shows that AT and A(-T) cases bearing truncation mutations of the ATM gene can produce modest amounts of full-length (and only rarely truncated) ATM protein. (nih.gov)
  • Most of these mutations lead to production of little or no functional p16(INK4A) protein. (medlineplus.gov)
  • The CDKN2A gene mutations found in melanoma result in a nonfunctional p16(INK4A) protein. (medlineplus.gov)
  • Together, the germline and somatic mutations impair the function of proteins that regulate division and senescence, leading to uncontrolled cell growth and the formation of a melanoma. (medlineplus.gov)
  • CDKN2A gene mutations involved in cancer impair production of functional p16(INK4A) or, less commonly, p14(ARF), which can result in uncontrolled cell growth and tumor formation. (medlineplus.gov)
  • Our recent report indicated that tumor suppressor gene ( p53 ) mutations and protein aberrant expression were detected in pterygium. (molvis.org)
  • A mutant p53 will no longer bind DNA in an effective way, and, as a consequence, the p21 protein will not be available to act as the "stop signal" for cell division. (wikipedia.org)
  • Another important function of p53 is to respond to environmental stimuli and help cells overcome difficulties caused by various stresses, including DNA damage, excessive ROS, and insufficient nutrients. (medicaltrend.org)
  • In cells, p53 is a very unstable protein with a short half-life. (medicaltrend.org)
  • We characterized the ATM protein expression in immortalized cells from AT and AT-variant patients, and heterozygotes and correlated it with two ATM-dependent radiation responses, G1 checkpoint arrest and p53-Ser 15 phosphorylation. (nih.gov)
  • Cells were transfected in six-well dishes as explained above by using 200 ng of a firefly luciferase reporter gene plasmid (pRGC, provided by M. Oren) that harbors a p53 DNA binding site in its promoter. (cancer-pictures.org)
  • Protein expression in living cells involves untethered intermediate molecules such as mRNA, enzymes, ribosomes, amino acids and polypeptides. (nature.com)
  • Proteins can also be expressed outside of living cells by subjecting gene DNA to 'cell-free' in vitro coupled transcription and translation (IVTT) reagent. (nature.com)
  • The uniformity of the numbers of terminal repeats (TRs) among EBV positive carcinoma cells reflects the clonal origin of a tumor and suggests that EBV is a causative virus for gastric carcinoma ( 6 ). (spandidos-publications.com)
  • All taken together, these observations underline the complexity of the mechanisms responsible for the selective destruction of proteins within cells. (cnrs.fr)
  • Both function as tumor suppressors, which means they keep cells from growing and dividing too rapidly or in an uncontrolled way. (medlineplus.gov)
  • Both proteins are also involved in stopping cell division in older cells (senescence). (medlineplus.gov)
  • The p14(ARF) and p53 proteins are often made in cells that are unable to undergo cell division. (medlineplus.gov)
  • Without p16(INK4A) to regulate cell growth and division (proliferation), cells can continue to grow and divide without control, which can lead to tumor formation. (medlineplus.gov)
  • Without one of these tumor suppressors, cells can grow and divide unchecked, leading to the development of cancer. (medlineplus.gov)
  • In this epithelium, as well as in the more fragile single cell layer epithelium of endocervix, the cells are held together by proteins that form desmosomes, tight junctions, and adherens junctions, which decrease its permeability [ 19 ]. (hindawi.com)
  • p53 has been characterized to play a role in blocking the proliferative action of damaged cells and act as an anticancer agent. (thermofisher.com)
  • p53 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. (thermofisher.com)
  • The tumor microenvironment refers to the surrounding microenvironment in which tumor cells exist, including the surrounding blood vessels, immune cells, fibroblasts, bone marrow-derived inflammatory cells, various signaling molecules, and extracellular matrix. (techscience.com)
  • Stress-response pathways play a key role in the patho-physiology and treatment of many diseases, including cancer.At almost every stage of the development of a tumour, cells are exposed to some form of stress. (southampton.ac.uk)
  • A particular interest of our work has been how HDM2 and HDMX protein synthesis is controlled in response to cell-signalling pathways in different cell types, and how this affects p53 function in these cells. (southampton.ac.uk)
  • EBV-LMPI expression in tumour cells of 10 of 26 cases of oesophageal carcinoma may also be of value in diagnosis and pathogenesis. (bvsalud.org)
  • Many tumor cells produce antigens, which may be released in the bloodstream or remain on the cell surface. (msdmanuals.com)
  • Tumor-associated antigens (TAAs) are relatively restricted to tumor cells. (msdmanuals.com)
  • Tumor-specific antigens (TSAs) are unique to tumor cells. (msdmanuals.com)
  • However, several antigens with selective expression on the surface of tumor cells are not associated with the major histocompatibility complex and may be candidates for therapeutic targeting. (msdmanuals.com)
  • References Many tumor cells produce antigens, which may be released in the bloodstream or remain on the cell surface. (msdmanuals.com)
  • By protecting p53, p14(ARF) also helps prevent tumor formation. (medlineplus.gov)
  • Most humoral responses cannot prevent tumor growth. (msdmanuals.com)
  • The principal objective of our broad, translational research is to determine structural attributes and to develop small-molecule compounds for new, emerging, cancer-related protein-protein interactions in the ubiquitin-proteasome system (UPS) and ubiquitin-like protein (UBL) conjugation pathways. (europa.eu)
  • Moreover, c-Fos, c-Jun and p53 turnovers are regulated upon activation of intracellular signalling cascades. (cnrs.fr)
  • Because environmental stimuli are often short-lived, p53 is required to function as quickly as possible, so stronger p53 activation is required. (medicaltrend.org)
  • The c-Fos and c-Jun oncoproteins and the p53 tumor suppressor protein are short-lived transcription factors. (cnrs.fr)
  • Using the PubMed database, Cochrane Library and Web of Science, studies published in English evaluating miRs differentially expressed in tumor tissue and significantly associated with the prognostic aspects of CRC were selected. (biorxiv.org)
  • The p21 protein binds directly to cyclin-CDK complexes that drive forward the cell cycle and inhibits their kinase activity, thereby causing cell cycle arrest to allow repair to take place. (wikipedia.org)
  • For example, a Nature article in Gu Wei's laboratory in 2016 found that the SET protein can selectively bind to the unacetylated C-terminal domain of p53 and inhibit the transcriptional activation function of p53. (medicaltrend.org)
  • The p21 gene contains several p53 response elements that mediate direct binding of the p53 protein, resulting in transcriptional activation of the gene encoding the p21 protein. (wikipedia.org)
  • A different type of alteration involving the CDKN2A gene can result in reduced amounts or an absence of the p16(INK4A) or p14(ARF) protein. (medlineplus.gov)
  • It can arrest growth by holding the cell cycle at the G1/S regulation point on DNA damage recognition-if it holds the cell here for long enough, the DNA repair proteins will have time to fix the damage and the cell will be allowed to continue the cell cycle. (wikipedia.org)
  • However, this limited expression of ATM protein provides no benefit regarding the ATM-dependent responses related to G1 arrest and p53-ser15 phosphorylation. (nih.gov)
  • Abstract Non-small cell lung cancer (NSCLC) is a malignant tumor with high incidence worldwide. (techscience.com)
  • We previously designed a p53 protein, p53FG, with amino substitutions S121F and V122G targeting loop L1. (rcsb.org)
  • The protein product of the murine double minute gene 2 (mdm-2) plays a central role in the regulation of p53. (lu.se)
  • Although some mechanisms through which TP inhibits NSCLC are well understood, those that involve ribosomal proteins remain yet to be understood. (techscience.com)
  • These in vitro, and their expression in these human tumour virus. (who.int)
  • The T category informs about tumor growth, depth and stage of adjacent tissues invasion. (biorxiv.org)
  • Epstein-Barr virus latent membrane protein expression and cyclin DI cell cyase protein expression in malignant and normal oesophageal tissues to see whether any variation in their expression in these tissues could be of diagnostic or prognostic value. (bvsalud.org)
  • Crystal structures of homo-oligomerizing p53 polypeptides with specific DNA suggest that DNA binding is associated with a conformational switch. (rcsb.org)
  • We use nuclear magnetic resonance (NMR) and X-ray crystallography techniques to structurally characterize protein-protein interactions (PPI) and to develop small-molecule inhibitors for these PPIs. (europa.eu)
  • One explanation is: if it can increase the level of p53, but also get rid of the negative regulation of transcription inhibitors, then the activation effect of p53 may be stronger. (medicaltrend.org)
  • The p53 proteins (originally thought to be, and often spoken of as, a single protein) are crucial in vertebrates, where they prevent cancer formation. (wikipedia.org)
  • Using the device to probe for an autoantibody cancer biomarker in blood serum sample gave five times higher signal to background ratio compared to standard protein microarray expressed on a flat microscope slide. (nature.com)
  • It also helped to open a very exciting avenue of research involving investigators with expertise in different aspects of growth control and cancer.Giordano's lab also discovered the tumor suppressor gene RB2/p130 and the cell cycle kinases CDK9 and CDK10, two other key players in cell cycle regulation and cell differentiation. (newswise.com)
  • They make up about one-third of proteins that human bodies make, Chen explains, and two-thirds of cancer-associated proteins contain large, disordered segments or domains. (umass.edu)
  • Toward that end, Chen's lab will study the molecular basis of how the anti-cancer drug EGCG, an antioxidant found in green tea extract, and their derivatives interact with the p53 gene, a tumor suppressor and the most important protein involved in cancer. (umass.edu)
  • page 42) paves the way for structure- based drug discovery to target the tumour suppressor p53 protein for potential cancer therapy. (esrf.fr)
  • The pTNM stage is a system of stage classification proposed by the American Joint Committee on Cancer which determines the degree of tumor development according with the T, N and M categories. (biorxiv.org)
  • In breast cancer patients, it is unclear whether measuring p53, mdm-2, or p21 expression provides information on how patients will respond to chemotherapy. (lu.se)
  • p53, mdm-2, p21, and mib-1 expression were assessed by immunohistochemical methods in primary tumors derived from 134 patients who took part in a randomized multicenter trial comparing docetaxel to sequential methotrexate and 5-fluorouracil (MF) in advanced breast cancer. (lu.se)
  • One exception is hu- humanized SCID mice, the use of al oncogenic viruses that are strictly man T-cell lymphotropic virus type 1 surrogate hosts has not proven very species-specific, causing cancer in (HTLV-1): in addition to its ability to useful for defining tumour site con- humans only. (who.int)
  • Animal models for human tumour mental animals is not easy to answer does induce adult T-cell leukaemia/ viruses that make use of animal virus- for these agents, because cancer bi- lymphoma (ATLL), albeit in monkeys es are scarce. (who.int)
  • Palmitic acid (PA) is the most common fatty acid in humans and mediates palmitoylation through its conversion into palmitoyl coenzyme A. Although palmitoylation affects many proteins, its pathophysiological functions are only partially understood. (researchgate.net)
  • For this reason, the infect humans, this virus can infect cordance between humans and ex- question about tumour site concor- several other species - including perimental animals. (who.int)
  • For other human tumour virus- primate species are related to the hu- tween data in humans and in experi- es, the use of humanized severe man tumour viruses, the incidence of mental animals is not obvious. (who.int)
  • This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag. (cusabio.com)
  • Moreover, The use of animals as surrogate rine host, can provide a platform for animal models for tumour viruses in hosts for the study of human tu- in vivo infection. (who.int)
  • The MIRA award enables us to continue working on several central problems regarding the study of disordered proteins and dynamic interactions. (umass.edu)
  • According to this model, it is speculated that if p53 can not be inhibited by various negative transcriptional regulatory proteins, even if its level is not significantly increased, it may be able to exert its normal tumor suppressor function. (medicaltrend.org)
  • PIAS did not exert any effects on sumoylation of the IB protein (Fig. (cancer-pictures.org)
  • The autophagophore membrane then elongates and encloses the molecules to be degraded forming an autophagosome, which occurs in two separate conjugation reactions catalyzed by autophagy-related proteins (ATGs). (hindawi.com)
  • Aifantis, I. Regulation of stem cell function by protein ubiquitylation. (benthamscience.com)
  • The authors observed: p53KQ/KQ mice will die in the perinatal period, mainly due to the activation of p53. (medicaltrend.org)
  • But p53KQ/- will also die before adulthood, because the activation of p53 causes hematopoietic dysfunction in p53KQ/- mice, and the mice die of ischemia. (medicaltrend.org)
  • He believed that the activation of p53 is not only due to the stability of its protein (increased protein level), but also due to the elimination of various negative regulatory binding proteins. (medicaltrend.org)
  • This indicates that the activation of p53 does not depend on the increase in the level of p53 protein, but as long as the inhibitory effect of transcription repressor protein is released. (medicaltrend.org)
  • 35S]Methionine-labeled translated proteins BGJ398 enzyme inhibitor were incubated with the relevant GST-fusion proteins loaded on glutathione-Sepharose 4b beads for 2 h at 4C in GST binding buffer (120 BGJ398 enzyme inhibitor mM NaCl/50 mM Tris, pH 8/0.25% Nonidet P-40/1 mM PMSF/1 mM DTT). (cancer-pictures.org)
  • To further examine whether the SUMO ligase activity of PIAS proteins is BGJ398 enzyme inhibitor restricted to p53, we tested several other SUMO targets in this system. (cancer-pictures.org)
  • Three more articles focus on the structural studies of key regulatory viral proteins to deepen our understanding in the infection cycles of the tick-borne encephalitis flavivirus (Rey et al. (esrf.fr)
  • In this cell type, p53 activates numerous microRNAs (like miR-302a, miR-302b, miR-302c, and miR-302d) that directly inhibit the p21 expression in hESCs. (wikipedia.org)
  • In situ protein expression for NAPPA is typically carried out on flat microscope slides by flooding the entire microarray surface with IVTT reagent. (nature.com)
  • p53, mdm-2, p21, and mib-1 expression were not significantly associated with response to chemotherapy, time to progression, or overall survival in the whole patient population or in the docetaxel group. (lu.se)
  • Interestingly, tumors with both negative mdm-2 and p21 expression, irrespective of p53 status, had a high response rate to docetaxel but no response to MF. (lu.se)
  • EBV-LMPI protein expression and cyclin DI expression were studied immunohisto chemically in these tissue sections. (bvsalud.org)
  • 2 cases of EBV-LMPI protein expression did not express p53 protein and 7 cases did not express both p53 and EBV-LMPI proteins. (bvsalud.org)
  • In a Cell review in 2009, he put forward a new view on the mechanism of p53. (medicaltrend.org)
  • Another 2011 study found that the p53 homozygous (Pro/Pro) genotype was associated with a significantly increased risk for renal cell carcinoma. (wikipedia.org)
  • His early research includes seminal work done in 1989, demonstrating the importance of cell cycle proteins in the functioning of DNA tumor viruses. (newswise.com)
  • Mitochondrial apoptotic priming is a key determinant of cell fate upon p53 restoration. (nih.gov)
  • These proteins help regulate the cell cycle, which is the cell's way of replicating itself in an organized, step-by-step fashion. (medlineplus.gov)
  • During elongation and maturation, the phagophore encapsulates damaged proteins and cell organelles. (hindawi.com)
  • To preserve protein function, assays using NAPPA are typically done within hours of expressing fresh proteins without ever allowing them to dry out. (nature.com)
  • High tumor proliferation has previously been associated with response to chemotherapy. (lu.se)
  • AMHERST, Mass. - Jianhan Chen , a University of Massachusetts Amherst chemistry and biochemistry and molecular biology professor, has received a five-year, $2 million National Institutes of Health (NIH) grant to support research in his computational biophysics lab aimed at better understanding the role of intrinsically disordered proteins (IDPs) in biology and human disease. (umass.edu)
  • Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and cause the loss of tumor suppressor activity. (thermofisher.com)
  • Inactivation of p53 by Human papillomavirus (HPV) 16/18 E6 plays a crucial role in cervical tumorigenesis. (molvis.org)