INVOLVED IN endosomal transport (ortholog); intracellular transport (ortholog); protein targeting (ortholog); FOUND IN cytosol (ortholog); endosome (ortholog); extracellular exosome (ortholog)
The classical Ras-association domain family (RASSF1-6) are a group of Ras effector molecules that contain a C-terminal Ras-association (RA) domain of the RalGDS/AF-6 variety and a protein interaction domain known as the Sav/RASSF/Hippo (SARAH) domain. Several members of the classical RASSF family are involved in tumorigenesis since epigenetic inactivation of many isoforms is a frequent event across many tumor types and their functions are consistent with roles as tumor suppressor proteins. Recently several additional RA-domain containing family members have been identified and designated N-terminal RASSF proteins (RASSF7-10). These comprise RASSF7 (also known as HRC1 located 11p15.5), RASSF8 (also known as HOJ-1 or C12ORF2 located 12p12.1), RASSF9 (also known as P-CIP1 or PAMCI located 12q21.31) and RASSF10 (located 11p15.2). These proteins are divergent and structurally distinct from RASSF1-6, containing an RA domain within their extreme N-termini and lacking the SARAH protein interaction ...
The mechanism by which Wnt receptors transduce signals to activate downstream beta-catenin-mediated target gene transcription remains incompletely understood but involves Frizzled (Fz) receptor-mediated plasma membrane recruitment and activation of the cytoplasmic effector Dishevelled (Dvl). Here, we identify the deubiquitinating enzyme CYLD, the familial cylindromatosis tumor suppressor gene, as a negative regulator of proximal events in Wnt/beta-catenin signaling. Depletion of CYLD from cultured cells markedly enhances Wnt-induced accumulation of beta-catenin and target gene activation. Moreover, we demonstrate hyperactive Wnt signaling in human cylindroma skin tumors that arise from mutations in CYLD. At the molecular level, CYLD interacts with and regulates K63-linked ubiquitination of Dvl. Enhanced ubiquitination of the polymerization-prone DIX domain in CYLD-deficient cells positively links to the signaling activity of Dvl. Together, our results argue that loss of CYLD instigates tumor growth in
Defective apoptosis contributes to the development of various human malignancies. The kinases nuclear Dbf2-related 1 (NDR1) and NDR2 mediate apoptosis downstream of the tumor suppressor proteins RASSF1A (Ras association domain family member 1A) and MST1 (mammalian Ste20-like kinase 1). To further analyze the role of NDR1 in apoptosis, we generated NDR1-deficient mice. Although NDR1 is activated by both intrinsic and extrinsic proapoptotic stimuli, which indicates a role for NDR1 in regulating apoptosis, NDR1-deficient T cells underwent apoptosis in a manner similar to that of wild-type cells in response to different proapoptotic stimuli. Analysis of the abundances of NDR1 and NDR2 proteins revealed that loss of NDR1 was functionally compensated for by an increase in the abundance of NDR2 protein. Despite this compensation, NDR1−/− and NDR1+/− mice were more prone to the development of T cell lymphomas than were wild-type mice. Tumor development in mice and humans was accompanied by a ...
Complete information for RASSF3 gene (Protein Coding), Ras Association Domain Family Member 3, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Complete information for RASSF8 gene (Protein Coding), Ras Association Domain Family Member 8, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
mouse Rassf3 protein: mouse homolog of the putative tumor suppressor gene RASSF1; about 60% homology at the amino acid level, possibly involved in Ras-like signaling pathways; RefSeq NM_138956
TSC22D4 is a member of the TSC22 domain family of leucine zipper transcriptional regulators (see TSC22D3; MIM 300506) (Kester et al., 1999 [PubMed 10488076]; Fiorenza et al., 2001 [PubMed 11707329]).[supplied by OMIM, Mar 2008 ...
GLTSCR1 - GLTSCR1 (untagged)-Human glioma tumor suppressor candidate region gene 1 (GLTSCR1) available for purchase from OriGene - Your Gene Company.
Cooperates with AGTR2 to inhibit ERK2 activation and cell proliferation. May be required for AGTR2 cell surface expression. Together with PTPN6, induces UBE2V2 expression upon angiotensin-II stimulation.
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
Homo sapiens Ras association (RalGDS/AF-6) domain family 1 (RASSF1), transcript variant F, mRNA. (H00011186-R06) - Products - Abnova
Homo sapiens Ras association (RalGDS/AF-6) domain family 5 (RASSF5), transcript variant 1, mRNA. (H00083593-R01) - Products - Abnova
MDDDDDSCLLDLIGDPQALNYFLHGPSNKSSNDDLTNAGYSAANSNSIFANSSNADPKSSLKGVSNQLGE 1 - 70 GPSDGLPLSSSLQFLEDELESSPLPDLTEDQPFDILQKSLQEANITEQTLAEEAYLDASIGSSQQFAQAQ 71 - 140 LHPSSSASFTQASNVSNYSGQTLQPIGVTHVPVGASFASNTVGVQHGFMQHVGISVPSQHLSNSSQISGS 141 - 210 GQIQLIGSFGNHPSMMTINNLDGSQIILKGSGQQAPSNVSGGLLVHRQTPNGNSLFGNSSSSPVAQPVTV 211 - 280 PFNSTNFQTSLPVHNIIIQRGLAPNSNKVPINIQPKPIQMGQQNTYNVNNLGIQQHHVQQGISFASASSP 281 - 350 QGSVVGPHMSVNIVNQQNTRKPVTSQAVSSTGGSIVIHSPMGQPHAPQSQFLIPTSLSVSSNSVHHVQTI 351 - 420 NGQLLQTQPSQLISGQVASEHVMLNRNSSNMLRTNQPYTGPMLNNQNTAVHLVSGQTFAASGSPVIANHA 421 - 490 SPQLVGGQMPLQQASPTVLHLSPGQSSVSQGRPGFATMPSVTSMSGPSRFPAVSSASTAHPSLGSAVQSG 491 - 560 SSGSNFTGDQLTQPNRTPVPVSVSHRLPVSSSKSTSTFSNTPGTGTQQQFFCQAQKKCLNQTSPISAPKT 561 - 630 TDGLRQAQIPGLLSTTLPGQDSGSKVISASLGTAQPQQEKVVGSSPGHPAVQVESHSGGQKRPAAKQLTK 631 - 700 GAFILQQLQRDQAHTVTPDKSHFRSLSDAVQRLLSYHVCQGSMPTEEDLRKVDNEFETVATQLLKRTQAM 701 - 770 LNKYRCLLLEDAMRINPSAEMVMIDRMFNQEERASLSRDKRLALVDPEGFQADFCCSFKLDKAAHETQFG 771 - 840 ...
Plasmid R777-E258 Hs.RASSF3-nostop from Dr. Dominic Espositos lab contains the insert RASSF3. This plasmid is available through Addgene.
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Canonical Wnt signaling is mediated by a molecular "switch" that regulates the transcriptional properties of the T-cell factor (TCF) family of DNA-binding proteins. Members of the myeloid translocation gene (MTG) family of transcriptional corepressors are frequently disrupted by chromosomal translocations in acute myeloid leukemia, whereas MTG16 may be inactivated in up to 40% of breast cancer and MTG8 is a candidate cancer gene in colorectal carcinoma. Genetic studies imply that this corepressor family may function in stem cells. Given that mice lacking Myeloid Translocation Gene Related-1 (Mtgr1) fail to maintain the secretory lineage in the small intestine, we surveyed transcription factors that might recruit Mtgr1 in intestinal stem cells or progenitor cells and found that MTG family members associate specifically with TCF4. Coexpression of beta-catenin disrupted the association between these corepressors and TCF4. Furthermore, when expressed in Xenopus embryos, MTG family members inhibited ...
A number of studies in lung cancer have shown that adjustments in the architecture of our DNA can result in chemo-resistance. Inactivation of RAS association domain family gene 2 (RASSF2; K-RAS adaptor protein) most commonly through promoter methylation, can confer a growth advantage in cancer cells having a K-RAS mutation. Both of these changes are common in lung cancer. Clark J et al. have determined that RASSF2 down regulation plays a role in cisplatin resistance [1]. Promoter hypermethylation of IGFBP-3 also encourages cisplatin resistance and it has been demonstrated that the basal methylation status of this gene may perhaps serve as a predictor to chemotherapy outcome [2]. In-depth promoter methylation analysis in the non-small cell lung cancer cell line A549, established significant differences in methylation patterns between its cisplatin resistant and sensitive subtypes. Significantly hypermethylated genes included G protein-coupled receptor 56 isoform 3 (GPR56), metallothionein 1G ...
Oncogenic signaling pathways in cellular transformation and apoptosis Carcinogenesis is a multi-step process that involves activation of proto-oncogenes and inactivation of tumor suppressor genes. Gain-of-function mutations in oncogenes are frequently detected in human cancers. Activation of oncogenes plays an important role in cancer development and in altering cellular sensitivities to anti-cancer agents. Research in my laboratory focuses on a number of areas: (1) Cellular kinases signaling in cancer cell proliferation, survival and death; (2) Studying the function and regulation of tumor suppressor RASSF1A; (3) Investigating the role of a novel family of GTPases, RBEL1A, B, C and D in regulation of cell death and proliferation; (4) Investigating the role of a novel growth suppresive lipase in cell growth control and cancer development; (5) Identification and development of novel anticancer agents using traditional Chinese medicines.. SELECTED PUBLICATIONS: Meltzer, S. J., Yin, J., Huang, Y., ...
Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterized by the widespread development of distinctive tumors termed hamartomas. TSC-determining loci have been mapped to chromosomes 9q34 (TSC1) and 16p13 (TSC2). TheTSC1 gene was identified from a 900-kilobase region containing at least 30 genes. The 8.6-kilobase TSC1transcript is widely expressed and encodes a protein of 130 kilodaltons (hamartin) that has homology to a putative yeast protein of unknown function. Thirty-two distinct mutations were identified inTSC1, 30 of which were truncating, and a single mutation (2105delAAAG) was seen in six apparently unrelated patients. In one of these six, a somatic mutation in the wild-type allele was found in a TSC-associated renal carcinoma, which suggests that hamartin acts as a tumor suppressor.. ...
Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterized by the widespread development of distinctive tumors termed hamartomas. TSC-determining loci have been mapped to chromosomes 9q34 (TSC1) and 16p13 (TSC2). TheTSC1 gene was identified from a 900-kilobase region containing at least 30 genes. The 8.6-kilobase TSC1transcript is widely expressed and encodes a protein of 130 kilodaltons (hamartin) that has homology to a putative yeast protein of unknown function. Thirty-two distinct mutations were identified inTSC1, 30 of which were truncating, and a single mutation (2105delAAAG) was seen in six apparently unrelated patients. In one of these six, a somatic mutation in the wild-type allele was found in a TSC-associated renal carcinoma, which suggests that hamartin acts as a tumor suppressor. ...
Full Text - CYLD is a deubiquitinating enzyme known for its role as a tumor suppressor whose mutation leads to skin appendages tumors and other cancers. In this manuscript we report that the tumor suppressor CYLD, similarly to other renowned tumor suppressor genes, protects from premature aging and cancer. We have generated transgenic mice expressing the mutant CYLDC/S protein, lacking its deubiquitinase function, under the control of the keratin 5 promoter, the K5-CYLDC/S mice. These mice express the transgene in different organs, including those considered to be more susceptible to aging, such as skin and thymus. Our results show that K5-CYLDC/S mice exhibit epidermal, hair follicle, and sebaceous gland alterations; and, importantly, they show signs of premature aging from an early age. Typically, 3-month-old K5-CYLDC/S mice exhibit a phenotype characterized by alopecia and kyphosis, and, the histological examination reveals that transgenic mice show signs
The mTOR/S6K/4E-BP1 pathway integrates extracellular signals derived from growth factors, and intracellular signals, determined by the availability of nutrients like amino acids and glucose. Activation of this pathway requires inhibition of the tumor suppressor complex TSC1/2. TSC2 is a GTPase-activ …
WWOX, WW domain-containing oxidoreductase, is a tumor suppressor that is altered in many human cancers, including breast cancer. Wwox interacts with the ErbB4 receptor, reduces nuclear translocation of the cleaved intracellular domain of ErbB4, and inhibits its transactivation function mediated thro …
Qiu, G.-H.,Lim, C.Y.,Tao, Q.,Tan, L.K.S.,Loh, K.S.,Srivastava, G.,Tsai, S.-T.,Tsao, S.W. (2004). The candidate tumor suppressor gene BLU, located at the commonly deleted region 3p21.3, is an E2F-regulated, stress-responsive gene and inactivated by both epigenetic and genetic mechanisms in nasopharyngeal carcinoma. Oncogene 23 (27) : 4793-4806. [email protected] Repository. https://doi.org/10.1038/sj.onc.1207632 ...
Deleted in malignant brain tumours 1 (DMBT1), a candidate tumour suppressor gene located on chromosome 10q25.3-q26.1, has recently been identified and found to be deleted in several different types of human tumours. In melanomas, the chromosomal regi
Our and others previous reports have demonstrated that the tumor suppressor DLEC1 is able to suppress cancer cell growth in vitro and in vivo (2, 6). The present study further confirmed the cell suppression function of DLEC1 by inducing G1 arrest and apoptosis in DLEC1 stable clones in colorectal cancer cell line HCT116. Induction of G1 arrest is a complex process, involving numerous factors. In addition to those tested in our study, others, such as p27 and pRb, also regulate G1/S transition (34). In this study, we found that over-expression of DLEC1 stimulated the expression of AP-2α2 (Figure 4), another tumor suppressor known to induce cell cycle arrest at G1 and apoptosis in various cancers (19-21). Therefore, cancer cell suppression by DLEC1 may be mediated through up-regulation of AP-2α2.. Nevertheless, given that DLEC1 is unlikely to be a transcription factor (Figure 1), and that AP-2α2 was up-regulated at transcriptional level by DLEC1 over-expression (Figure 4), DLEC1 is not likely ...
Gene silencing suppressor 2b complexed with silencing RNA (ribonucleic acid). Computer model showing the structure of the gene silencing suppressor 2b (purple, green) complexed with synthetic silencing RNA (yellow, magenta). From Tomato aspermy virus. - Stock Image C035/8421
Oncogenes and tumor suppressor genes (TSGs) both play a role in oncogenesis via opposite mechanisms. Proto-oncogenes promote normal cell growth. Occasionally, a mutation increases their activity or a duplication, translocation, or other genetic event increases their expression. Under such conditions, these genes, now called oncogenes, cause abnormal unchecked cell growth. Examples of proto-oncogenes include growth factors, tyrosine kinases, regulatory GTPases, and transcription factors. TSGs inhibit cell growth in normal cells. However, decreases in TSG activity, often caused by mutation or promoter hypermethylation, prevents their ability to stop abnormal cell growth. Examples of TSGs include genes that regulate apoptosis, cell adhesion, or DNA damage signaling. Genes may have oncogenic properties, tumor suppressor properties, or both. These properties depend not only on the tumor type, but also on the known or observed differences in gene expression or epigenetic marks. Genetic differences in ...
In most myeloid leukemias induced in mice by γ-radiation, one copy of chromosome 2 has suffered a deletion. To search for a potential tumor suppressor gene in that region, we have delineated the deletions in a panel of these tumors. A commonly deleted region of 2 megabase pairs (Mbp) includes the gene encoding the PU.1 transcription factor, a powerful inducer of granulocytic/monocytic differentiation. Significantly, in 87% of these tumors the remaining PU.1 allele exhibited point mutations in the PU.1 DNA binding domain. Surprisingly, 86% of these mutations altered a single CpG, implicating deamination of deoxycytidine, a common mutational mechanism, as the origin of this lesion. The "hot spot" resides in the codon for a contact residue essential for DNA binding by PU.1. In keeping with a tumor suppressor role for PU.1, enforced expression of wild-type PU.1 in the promyelocytic leukemia cells inhibited their clonogenic growth, induced monocytic differentiation, and elicited apoptosis. The ...
The tuberous sclerosis 1 (TSC1) gene in humans encodes a peripheral membrane protein also known as hamartin, TSC, LAM, and KIAA0243. TSC1 complexes with TSC2 (tuberin) and stabilizes it. The TSC1/TSC2 complex inhibits the nutrient-mediated or growth factor-stimulated phosphorylation of eukaryotic translation initiation factor 4E-binding protein 1 (EIF4BP1) and ribosomal protein S6 kinase (S6K1), by negatively regulating signaling in the mammalian target of rapamycin complex 1 (mTORC1). Mutations in the TSC1 gene are associated with the development of tuberous sclerosis.. ...
The tuberous sclerosis 1 (TSC1) gene in humans encodes a peripheral membrane protein also known as hamartin, TSC, LAM, and KIAA0243. TSC1 complexes with TSC2 (tuberin) and stabilizes it. The TSC1/TSC2 complex inhibits the nutrient-mediated or growth factor-stimulated phosphorylation of eukaryotic translation initiation factor 4E-binding protein 1 (EIF4BP1) and ribosomal protein S6 kinase (S6K1), by negatively regulating signaling in the mammalian target of rapamycin complex 1 (mTORC1). Mutations in the TSC1 gene are associated with the development of tuberous sclerosis.. ...
SnoN is a negative regulator of TGF-β signaling and also an activator of the tumor suppressor p53 in response to cellular stress. Its role in human cancer is complex and controversial with both pro-oncogenic and anti-oncogenic activities reported. To clarify its role in human cancer and provide clinical relevance to its signaling activities, we examined SnoN expression in normal and cancerous human esophageal, ovarian, pancreatic and breast tissues. In normal tissues, SnoN is expressed in both the epithelium and the surrounding stroma at a moderate level and is predominantly cytoplasmic. SnoN levels in all tumor epithelia examined are lower than or similar to that in the matched normal samples, consistent with its anti-tumorigenic activity in epithelial cells. In contrast, SnoN expression in the stroma is highly upregulated in the infiltrating inflammatory cells in high-grade esophageal and ovarian tumor samples, suggesting that SnoN may potentially promote malignant progression through ...
You have 2 copies of most genes - one from each parent. When someone has inherited an abnormal copy of a gene, their cells already start out with one mutation. If the other copy of the gene stops working (because of an acquired mutation, for example), the gene can stop functioning altogether. When the gene that stops working is a cancer susceptibility gene, cancer can develop. Some cancer susceptibility genes function as tumor suppressor genes. Tumor suppressor genes are normal genes that slow down cell division, repair DNA mistakes, or tell cells when to die (a process known as apoptosis or programmed cell death). When tumor suppressor genes dont work properly, cells can grow out of control, which can lead to cancer. Many family cancer syndromes are caused by inherited defects of tumor suppressor genes ...
LATS1 tumor suppressor is a serine/threonine kinase of the AGC kinase family and a core component of the Hippo pathway in mammals. LATS1 regulates various biological processes such as cell cycle progression, genetic stability, cell motility and adhesion, apoptosis, stem cell renewal and differentiation (Visser and Yang, 2010; Mo et al., 2014). LATS1 performs these functions by phosphorylating various substrates such as transcriptional co-activators YAP and TAZ (Zhao et al., 2007; Hao et al., 2008). LATS1 is also required for tissue homeostasis in both flies and mice (Visser et al., 2010). In addition to its roles in a broad spectrum of normal biological processes, loss of LATS1 has been shown to be important for the development of cancer and resistance to chemotherapeutic drugs (Visser et al., 2010). Therefore, understanding the molecular mechanisms underlying loss-of-LATS1-induced tumorigenesis and drug resistance will shed light on the design of new cancer treatment strategies in the future ...
References for Abcams Recombinant Human WWOX protein (ab86687). Please let us know if you have used this product in your publication
Lowe, S. (November 2002) Roles of oncogenes and tumor suppressor genes in apoptosis. European Journal of Cancer, 38. S15-S15. ISSN 0959-8049 ...
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Powerful new tools are now available to discover and understand tumor suppressor genes (TSGs) and the biochemical mechanisms by which they control cancer
(2012) Gannon et al. Cancer Cell. DNA damage induced by ionizing radiation activates the ATM kinase, which subsequently stabilizes and activates the p53 tumor suppressor protein. Although phosphorylation of p53 by ATM was found previously to modulate p53 levels and transcriptional activities in v...
Colorectal Cancer (CRC) is a genetic disease in which progression is driven by the accumulation of mutations or epigenetic alterations in oncogenes and tumor su...
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no danger of their falling : Some names of things have an -ing form, though no -ed, and sometimes no -er form. Fall has only the -ing form. Drinking and running are two other examples used in this Step. Drink and run may, in addition, take -er. -- Take note that the person or thing in relation to which an -ing form is used, if not the same as the doer of the operation in the statement, has to be made clear by using an owner-form ...
Mouse anti PTEN tumour suppressor antibody, clone A2b1, is specific for PTEN, a tumour suppressor protein located on the human chromosome