A nucleocytoplasmic transport protein that binds to ALPHA KARYOPHERINS and RAN GTP BINDING PROTEIN inside the CELL NUCLEUS and participates in their export into CYTOPLASM. It is also associated with the regulation of APOPTOSIS and microtubule assembly.
A plant genus of the family POLYGONACEAE. Members contain chrysophanic acid, rhein, EMODIN, and other ANTHRAQUINONES. The roots were formerly used as PURGATIVES.
A family of highly conserved serine-threonine kinases that are involved in the regulation of MITOSIS. They are involved in many aspects of cell division, including centrosome duplication, SPINDLE APPARATUS formation, chromosome alignment, attachment to the spindle, checkpoint activation, and CYTOKINESIS.
An aurora kinase that localizes to the CENTROSOME during MITOSIS and is involved in centrosome regulation and formation of the MITOTIC SPINDLE. Aurora A overexpression in many malignant tumor types suggests that it may be directly involved in NEOPLASTIC CELL TRANSFORMATION.
An aurora kinase that is a component of the chromosomal passenger protein complex and is involved in the regulation of MITOSIS. It mediates proper CHROMOSOME SEGREGATION and contractile ring function during CYTOKINESIS.
Aurora kinase C is a chromosomal passenger protein that interacts with aurora kinase B in the regulation of MITOSIS. It is found primarily in GERM CELLS in the TESTIS, and may mediate CHROMOSOME SEGREGATION during SPERMATOGENESIS.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.

Evidence for distinct substrate specificities of importin alpha family members in nuclear protein import. (1/50)

Importin alpha plays a pivotal role in the classical nuclear protein import pathway. Importin alpha shuttles between nucleus and cytoplasm, binds nuclear localization signal-bearing proteins, and functions as an adapter to access the importin beta-dependent import pathway. In contrast to what is found for importin beta, several isoforms of importin alpha, which can be grouped into three subfamilies, exist in higher eucaryotes. We describe here a novel member of the human family, importin alpha7. To analyze specific functions of the distinct importin alpha proteins, we recombinantly expressed and purified five human importin alpha's along with importin alpha from Xenopus and Saccharomyces cerevisiae. Binding affinity studies showed that all importin alpha proteins from humans or Xenopus bind their import receptor (importin beta) and their export receptor (CAS) with only marginal differences. Using an in vitro import assay based on permeabilized HeLa cells, we compared the import substrate specificities of the various importin alpha proteins. When the substrates were tested singly, only the import of RCC1 showed a strong preference for one family member, importin alpha3, whereas most of the other substrates were imported by all importin alpha proteins with similar efficiencies. However, strikingly different substrate preferences of the various importin alpha proteins were revealed when two substrates were offered simultaneously.  (+info)

Recycling of importin alpha from the nucleus is suppressed by loss of RCC1 function in living mammalian cells. (2/50)

We previously reported that the nuclear import of substrates containing SV40 T antigen nuclear localization signal (NLS) was suppressed in a temperature-sensitive RCC1 mutant cell line, tsBN2, at nonpermissive temperature. Moreover, it was shown that import into wild type BHK21 cell-derived nuclei gradually decreased in heterokaryons between the tsBN2 and BHK21 cells, although the BHK21 nuclei retained wild type RCC1 and should contain RanGTP (Tachibana et al., 1994). In this study, it was found that in the heterokaryons cultured at non-permissive temperature, endogenous importin alpha was not detected immunocytochemically in the cytoplasm or BHK21 nuclei but only in the tsBN2 nuclei, suggesting that importin alpha cannot be exported from the RCC1-depleted nuclei. In fact, importin alpha microinjected into the nucleus of tsBN2 cells at non-permissive temperature remained in the nucleus. These results strongly support the hypothesis that the recycling of importin alpha from the nucleus requires nuclear RanGTP. Moreover, it was found that cytoplasmic injection of importin alpha restored the import of SV40 T-NLS substrates in the BHK21 nuclei but not the tsBN2 nuclei in the heterokaryons. This indicates that the decrease of importin alpha from the cytoplasm in the heterokaryons leads to a suppression of the efficiency of nuclear import of the T-NLS substrate and provides support for the view that nuclear RanGTP is essential for the nuclear entry of the substrates.  (+info)

Nup50, a nucleoplasmically oriented nucleoporin with a role in nuclear protein export. (3/50)

We present here a detailed analysis of a rat polypeptide termed Nup50 (formerly NPAP60) that was previously found to be associated with the nuclear pore complex (F. Fan et al., Genomics 40:444-453, 1997). We have found that Nup50 (and/or a related 70-kDa polypeptide) is present in numerous rat cells and tissues. By immunofluorescence microscopy, Nup50 was found to be highly concentrated at the nuclear envelope of rat liver nuclei, whereas in cultured NRK cells it also is abundant in intranuclear regions. On the basis of immunogold electron microscopy of both rat liver nuclear envelopes and NRK cells, we determined that Nup50 is specifically localized in the nucleoplasmic fibrils of the pore complex. Microinjection of anti-Nup50 antibodies into the nucleus of NRK cells resulted in strong inhibition of nuclear export of a protein containing a leucine-rich nuclear export sequence, whereas nuclear import of a protein containing a classical nuclear localization sequence was unaffected. Correspondingly, CRM1, the export receptor for leucine-rich export sequences, directly bound to a fragment of Nup50 in vitro, whereas several other import and export receptors did not significantly interact with this fragment. Taken together, our data indicate that Nup50 has a direct role in nuclear protein export and probably serves as a binding site on the nuclear side of the pore complex for export receptor-cargo complexes.  (+info)

G(i)-mediated Cas tyrosine phosphorylation in vascular endothelial cells stimulated with sphingosine 1-phosphate: possible involvement in cell motility enhancement in cooperation with Rho-mediated pathways. (4/50)

Since blood platelets release sphingosine 1-phosphate (Sph-1-P) upon activation, it is important to examine the effects of this bioactive lipid on vascular endothelial cell functions from the viewpoint of platelet-endothelial cell interactions. In the present study, we examined Sph-1-P-stimulated signaling pathways related to human umbilical vein endothelial cell (HUVEC) motility, with a special emphasis on the cytoskeletal docking protein Crk-associated substrate (Cas). Sph-1-P stimulated tyrosine phosphorylation of Cas, which was inhibited by the G(i) inactivator pertussis toxin but not by the Rho inactivator C3 exoenzyme or the Rho kinase inhibitor Y-27632. Fyn constitutively associated with and phosphorylated Cas, suggesting that Cas tyrosine phosphorylation may be catalyzed by Fyn. Furthermore, upon HUVEC stimulation with Sph-1-P, Crk, through its SH2 domain, interacted with tyrosine-phosphorylated Cas, and the Cas-Crk complex translocated to the cell periphery (membrane ruffles), through mediation of G(i) (Fyn) but not Rho. In contrast, tyrosine phosphorylation of focal adhesion kinase, and formation of stress fibers and focal adhesion were mediated by Rho but not G(i) (Fyn). Finally, Sph-1-P-enhanced HUVEC motility, assessed by a phagokinetic assay using gold sol-coated plates and a Boyden's chamber assay, was markedly inhibited not only by pertussis toxin (or the Fyn kinase inhibitor PP2) but also by C3 exoenzyme (or Y-27632). In HUVECs stimulated with Sph-1-P, these data suggest the following: (i) cytoskeletal signalings may be separable into G(i)-mediated signaling pathways (involving Cas) and Rho-mediated ones (involving FAK), and (ii) coordinated signalings from both pathways are required for Sph-1-P-enhanced HUVEC motility. Since HUVECs reportedly express the Sph-1-P receptors EDG-1 (coupled with G(i)) and EDG-3 (coupled with G(13) and G(q)) and the EDG-3 antagonist suramin was found to block specifically Rho-mediated responses, it is likely that Cas-related responses following G(i) activation originate from EDG-1, whereas Rho-related responses originate from EDG-3.  (+info)

Identification of residues in the N-terminal domain of the Yersinia tyrosine phosphatase that are critical for substrate recognition. (5/50)

YopH is a 468-amino acid protein-tyrosine phosphatase that is produced by pathogenic Yersinia species. YopH is translocated into host mammalian cells via a type III protein secretion system. Translocation of YopH into human epithelial cells results in dephosphorylation of p130(Cas) and paxillin, disruption of focal adhesions, and inhibition of integrin-mediated bacterial phagocytosis. Previous studies have shown that the N-terminal 129 amino acids of YopH comprise a bifunctional domain. This domain binds to the SycH chaperone in Yersinia to orchestrate translocation and to tyrosine-phosphorylated target proteins in host cells to mediate substrate recognition. We used random mutagenesis in combination with the yeast two-hybrid system to identify residues in the YopH N-terminal domain that are involved in substrate-binding activity. Four single codon changes (Q11R, V31G, A33D, and N34D) were identified that interfered with binding of the YopH N-terminal domain to tyrosine-phosphorylated p130(Cas) but not to SycH. These mutations did not impair YopH translocation into HeLa cells infected with Yersinia pseudotuberculosis. Introduction of the V31G substitution into catalytically inactive (substrate-trapping) forms of YopH interfered with the ability of these proteins to bind to p130(Cas) and to localize to focal adhesions in HeLa cells. In addition, the V31G substitution reduced the ability of catalytically active YopH to dephosphorylate target proteins in HeLa cells. These data indicate that the substrate- and SycH-binding activities of the YopH N-terminal domain can be separated and that the former activity is important for recognition and dephosphorylation of substrates by YopH in vivo.  (+info)

Cse1l is essential for early embryonic growth and development. (6/50)

The CSE1L gene, the human homologue of the yeast chromosome segregation gene CSE1, is a nuclear transport factor that plays a role in proliferation as well as in apoptosis. CSE1 and CSE1L are essential genes in Saccharomyces cerevisiae and mammalian cells, as shown by conditional yeast mutants and mammalian cell culture experiments with antisense-mediated depletion of CSE1L. To analyze whether CSE1L is also essential in vivo and whether its absence can be compensated for by other genes or mechanisms, we have cloned the murine CSE1L gene (Cse1l) and analyzed its tissue- and development-specific expression: Cse1l was detected at embryonic day 7.0 (E7.0), E11.0, E15.0, and E17.0, and in adults, high expression was observed in proliferating tissues. Subsequently, we inactivated the Cse1l gene in embryonic stem cells to generate heterozygous and homozygous knockout mice. Mice heterozygous for Cse1l appear normal and are fertile. However, no homozygous pups were born after interbreeding of heterozygous mice. In 30 heterozygote interbreeding experiments, 50 Cse1l wild-type mice and 100 heterozygotes were born but no animal with both Cse1l alleles deleted was born. Embryo analyses showed that homozygous mutant embryos were already disorganized and degenerated by E5.5. This implicates with high significance (P < 0.0001, Pearson chi-square test) an embryonically lethal phenotype of homozygous murine CSE1 deficiency and suggests that Cse1l plays a critical role in early embryonic development.  (+info)

Functions of the adapter protein Cas: signal convergence and the determination of cellular responses. (7/50)

Since Cas was first identified as a highly phosphorylated 130 kilodalton protein that associated with the v-Src and v-Crk-oncoproteins, considerable effort has been made to determine its function. Its predicted role as a scaffolding molecule based on its domain structure has been largely confirmed. Through its ability to undergo rapid changes in phosphorylation, subcellular localization and association with heterologous proteins, Cas may spatially and temporally regulate the function of its binding partners. Numerous proteins have been identified that bind to Cas in vitro and/or in vivo, but in only a few cases is there an understanding of how Cas may function in these protein complexes. To date, Cas-Crk and Cas-Src complexes have been most frequently implicated in Cas function, particularly in regards to processes involving regulation of the actin cytoskeleton and proliferation. These and other Cas protein complexes contribute to the critical role of Cas in cell adhesion, migration, proliferation and survival of normal cycling cells. However, under conditions in which these processes are deregulated, Cas appears to play a role in oncogenic transformation and perhaps metastasis. Therefore, in its capacity as an adapter protein, Cas serves as a point of convergence for many distinct signaling inputs, ultimately contributing to the generation of specific cellular responses.  (+info)

Characterization of the nuclear export signal of polypyrimidine tract-binding protein. (8/50)

The polypyrimidine tract-binding protein (PTB) is a nuclear protein that regulates alternative splicing. In addition, it plays a role in the cytoplasm during infection by some viruses and functions as a positive effector of hepatitis B virus RNA export. Thus, it presumably contains a nuclear export signal (NES). Using a heterokaryon export assay in transfected cultured cells, we have shown that the N-terminal 25 amino acid residues of PTB function as an autonomous NES, with residues 11-16 being important for its activity. Unlike the heteronuclear ribonucleoprotein A1 NES, this NES is separable from the nuclear localization signal, which spans the entire N-terminal 60 residues of PTB. The PTB NES cannot be shown to bind to CAS or Crm1, cellular receptors known to export proteins from the nucleus, and it functions in the presence of leptomycin B, a specific inhibitor of Crm1-dependent export. PTB deleted of its NES, unlike wild type PTB, does not stimulate the export of hepatitis B virus RNA. Therefore, the PTB NES is a functionally important domain of this multifunctional protein that utilizes an unknown export receptor.  (+info)

The Cellular Apoptosis Susceptibility Protein, also known as Apaf-1 (Apoptotic Protease Activating Factor 1), is a protein that plays a crucial role in the regulation of programmed cell death, or apoptosis. It is involved in the intrinsic pathway of apoptosis, which is initiated by various intracellular signals such as DNA damage and oxidative stress.

Apaf-1 is located in the cytoplasm and functions as a molecular adaptor that brings together several proteins to form the apoptosome complex. When activated, Apaf-1 binds to cytochrome c, which is released from damaged mitochondria, and ATP or dATP to form the apoptosome. The apoptosome then recruits and activates caspase-9, a protease that cleaves and activates other downstream caspases, leading to the ordered dismantling of the cell.

Mutations in the Apaf-1 gene have been associated with various human diseases, including neurodegenerative disorders and cancer. In some cases, mutations in Apaf-1 can lead to a decreased ability to undergo apoptosis, which can contribute to tumor development and resistance to chemotherapy. On the other hand, increased activity of Apaf-1 has been implicated in excessive apoptosis and neurodegeneration.

In medical terms, "Rheum" is not a specific disease or condition. Instead, it is a term that was historically used to refer to a variety of disorders characterized by inflammation and pain in the musculoskeletal system, particularly in the joints. These disorders were often associated with symptoms such as stiffness, swelling, and warmth in the affected areas.

Over time, the term "rheumatic diseases" has become more commonly used to describe this group of conditions. Rheumatic diseases now encompass a wide range of disorders that affect the joints, muscles, tendons, ligaments, bones, and other connective tissues. Examples include rheumatoid arthritis, osteoarthritis, lupus, gout, and many others.

It's important to note that while "rheum" is an outdated term in modern medical nomenclature, it still holds historical significance and is sometimes used in the names of certain medical conditions or concepts, such as "rheumatology," which is the medical specialty focused on the diagnosis and management of rheumatic diseases.

Aurora kinases are a family of serine/threonine protein kinases that play crucial roles in the regulation of cell division. There are three members of the Aurora kinase family, designated as Aurora A, Aurora B, and Aurora C. These kinases are involved in the proper separation of chromosomes during mitosis and meiosis, and their dysregulation has been implicated in various types of cancer.

Aurora A is primarily located at the centrosomes and spindle poles during cell division, where it regulates centrosome maturation, bipolar spindle formation, and chromosome segregation. Aurora B, on the other hand, is a component of the chromosomal passenger complex (CPC) that localizes to the centromeres during prophase and moves to the spindle midzone during anaphase. It plays essential roles in kinetochore-microtubule attachment, chromosome alignment, and cytokinesis. Aurora C is most similar to Aurora B and appears to have overlapping functions with it, although its specific roles are less well understood.

Dysregulation of Aurora kinases has been associated with various types of cancer, including breast, ovarian, colon, and lung cancers. Overexpression or amplification of Aurora A is observed in many cancers, leading to chromosomal instability and aneuploidy. Inhibition of Aurora kinases has emerged as a potential therapeutic strategy for cancer treatment, with several small molecule inhibitors currently under investigation in clinical trials.

Aurora Kinase A is a type of serine/threonine kinase that plays a crucial role in the regulation of cell division and mitosis. It is encoded by the AURKA gene in humans. This enzyme is responsible for proper chromosome alignment and segregation during mitosis, and its dysregulation has been implicated in various types of cancer. Aurora Kinase A is often overexpressed in cancer cells, leading to chromosomal instability and aneuploidy, which contribute to tumor growth and progression. Inhibitors of Aurora Kinase A are being investigated as potential cancer therapeutics.

Aurora Kinase B is a type of enzyme that plays a crucial role in the regulation of cell division and mitosis. It is a member of the Aurora kinase family, which includes three different isoforms (Aurora A, B, and C). Among these, Aurora Kinase B is specifically involved in the proper alignment and separation of chromosomes during cell division.

During mitosis, Aurora Kinase B forms a complex with other proteins to form the chromosomal passenger complex (CPC), which plays a critical role in ensuring accurate chromosome segregation. The CPC is responsible for regulating various events during mitosis, including the attachment of microtubules to kinetochores (protein structures that connect chromosomes to spindle fibers), the correction of erroneous kinetochore-microtubule attachments, and the regulation of the anaphase promoting complex/cyclosome (APC/C), which targets specific proteins for degradation during mitosis.

Dysregulation of Aurora Kinase B has been implicated in various human diseases, including cancer. Overexpression or amplification of this kinase can lead to chromosomal instability and aneuploidy, contributing to tumorigenesis and cancer progression. As a result, Aurora Kinase B is considered a promising target for the development of anti-cancer therapies, with several inhibitors currently being investigated in preclinical and clinical studies.

Aurora Kinase C is a type of serine/threonine protein kinase that is involved in the regulation of cell division and mitosis. It plays a crucial role in the proper separation of chromosomes during cell division, ensuring the genetic stability of cells. Mutations in the gene that encodes Aurora Kinase C have been associated with various types of cancer, including colon, breast, and ovarian cancers. Inhibitors of Aurora Kinase C are being studied as potential cancer therapeutics.

Rheumatoid arthritis (RA) is a systemic autoimmune disease that primarily affects the joints. It is characterized by persistent inflammation, synovial hyperplasia, and subsequent damage to the articular cartilage and bone. The immune system mistakenly attacks the body's own tissues, specifically targeting the synovial membrane lining the joint capsule. This results in swelling, pain, warmth, and stiffness in affected joints, often most severely in the hands and feet.

RA can also have extra-articular manifestations, affecting other organs such as the lungs, heart, skin, eyes, and blood vessels. The exact cause of RA remains unknown, but it is believed to involve a complex interplay between genetic susceptibility and environmental triggers. Early diagnosis and treatment are crucial in managing rheumatoid arthritis to prevent joint damage, disability, and systemic complications.

Protein-Serine-Threonine Kinases (PSTKs) are a type of protein kinase that catalyzes the transfer of a phosphate group from ATP to the hydroxyl side chains of serine or threonine residues on target proteins. This phosphorylation process plays a crucial role in various cellular signaling pathways, including regulation of metabolism, gene expression, cell cycle progression, and apoptosis. PSTKs are involved in many physiological and pathological processes, and their dysregulation has been implicated in several diseases, such as cancer, diabetes, and neurodegenerative disorders.

  • The Cas family of proteins are a family of proteins that induce cellular apoptosis and cell proliferation. (wikipedia.org)
  • Cas is a 2 terminal protein, a N-terminal and a C-terminal, and there is a positive correlation between the presence of CAS and the degree of cellular proliferation. (wikipedia.org)
  • The cellular apoptosis susceptibility protein (CAS) is the human homologue of the product of the essential yeast chromosome segregation gene, CSE1, and has important roles in tumor necrosis factor (TNF)-induced apoptosis and cell proliferation. (nih.gov)
  • 15. Apoptosis and proliferation in relation to histopathological variables and prognosis in hepatocellular carcinoma. (nih.gov)
  • HPV-infected cells express some viral proteins encoded by genes called E6 and E7, and can inactivate p53 protein and the retinoblastoma-type guerison hpv apres conisation RBP involved in the regulation of proliferation and cell death. (alexandrudiaconescu.ro)
  • VSMCs can synthesize and secrete biologically active mediators that regulate contraction and relaxation, inflammation, proliferation, apoptosis and matrix alterations (Fig. 3). (medscape.com)
  • Moreover, there is increasing evidence that connections exist between proliferation and other cellular processes that are important for the pathophysiology of vascular disease. (medscape.com)
  • For example, macrophage migration inhibitory factor, which is essential in several inflammatory conditions, stabilizes the cell cycle-inhibitory protein p27 KIP1 and blocks proliferation. (medscape.com)
  • Notch activity is related to general growth stages such as organogenesis and morphogenesis and has effects on cell differentiation, cell proliferation, and apoptosis. (ksbu.edu.tr)
  • Lung cancer associated with degradation of proteins which regulate cellular activities such as cell growth, differentiation, proliferation and apoptosis or the loss of function of proteins due to mutations in the genes which that express these proteins. (ksbu.edu.tr)
  • HPV16 E6-T295/T350, G295/G350, and T295/G350 GV230 vectors were stably transfected into cervical cancer C33A cells to analyze the cell proliferation, migration and invasion, apoptosis by CCK8 and clonogenic assays, transwell and cell scratch assays, FACS experiments. (biomedcentral.com)
  • When E6 vector(s) of mutations sites were transfected into C33A cells, they were found to promote cellular proliferation, migration, invasion, and inhibit apoptosis. (biomedcentral.com)
  • This is particularly important as UPR downregulate essential processes of the endochondral ossification including chondrocyte proliferation and differentiation and ECM protein synthesis. (hindawi.com)
  • Previous studies indicate that miRNAs play a very important role in determining cellular development, apoptosis, differentiation, and proliferation. (biomedcentral.com)
  • Insulin-like growth factor 1 is known as peptide growth factor found to increase the proliferation of cell and prevent apoptosis. (springeropen.com)
  • The IGF family performs cell proliferation and inhibits apoptosis and influence cell transformation through regulatory proteins synthesis [ 11 ]. (springeropen.com)
  • This protein induces transcription of genes that activate cell cycle checkpoints or induce apoptosis. (nih.gov)
  • The key genes were screened from DEGs to establish a multiscale embedded gene co-expression network, protein-protein interaction network, and survival analysis. (biomedcentral.com)
  • MicroRNAs (miRNAs) are a newly discovered type of small non-protein coding RNA that function in the inhibition of effective mRNA translation, and may serve as susceptibility genes for various disease developments. (biomedcentral.com)
  • miRNA targets are largely unknown but they are thought to target about 30%-80% of total human proteins at a frequency of about one to hundreds of target genes for a given miRNA. (biomedcentral.com)
  • A long search for the gene(s) responsible for diabetes susceptibility has identified only very few candidate genes in past decades. (biomedcentral.com)
  • Given miRNA's suppressive nature and critical role in regulation, the possibility that miRNAs are T1D-risk genes may underlie the diverse findings of genetic studies, including evidence that protein altering gene polymorphisms are not generally found in T1D. (biomedcentral.com)
  • Functional polymorphisms in apoptosis pathway genes and survival in patients with gastric cancer. (cdc.gov)
  • HPV is a non-enveloped, double-stranded DNA virus from the family of Papillomaviridae, with an 8 kb circular genome composed of six early ORFs open reading frames with role in viral transcription and replication E1, E2, E4, E5, E6, E7two late ORFs L1,2-capsid proteins and a non-coding long controlled region LCR that contains a variety of cis elements, which regulate viral replication and gene expression. (constiintaortodoxa.ro)
  • By cloning and sequencing a very likely candidate gene (based on knowledge of the receptor that results in susceptibility), Klucking et al. (omia.org)
  • Through my thesis work, I have investigated beta cell-specific etiologies of T1D through both a candidate-based approach using beta cell specific deletion of a susceptibility gene and an unbiased global exploration of beta cell factors that regulate the predisposition to insulitic injury. (columbia.edu)
  • Protein tyrosine phosphatase N2 (PTPN2) is a T1D candidate gene that has been shown to be critical for modulating inflammation by regulating T cell activation. (columbia.edu)
  • In an attempt to test whether miR-938 may be a susceptibility gene for IDDM10, we assessed the possible association of the miR-938 SNP with T1D in an American Caucasian cohort of 622 patients and 723 healthy controls by TaqMan assay. (biomedcentral.com)
  • Mutations located in critical areas of the mature miRNA potentially affect its structure or expression level, which may lead to abnormal protein-coded gene expression that is phenotypically similar to the disruption of the protein-coded gene itself. (biomedcentral.com)
  • Thus, inadequate or miss-timed expression of a functional protein may occur either due to disruption of the DNA coding sequence, leading to a dysfunctional protein, or due to abnormal miRNA regulation of a normal gene. (biomedcentral.com)
  • The results of this study support the hypothesis that changes to cis -regulation of gene expression are involved in a large proportion of SNP associations with type 2 diabetes susceptibility. (diabetesjournals.org)
  • Similar to other complex polygenic diseases, the lack of protein-coding variation at the majority of these loci has led many to believe that the disease-associated variation must result in changes in the level of gene expression. (diabetesjournals.org)
  • Association study of polymorphisms in the receptor for advanced glycation end-products (RAGE) gene with susceptibility and prognosis of heart failure. (cdc.gov)
  • Hence, the study aimed to find association of IGF-1 rs6214(C/T) gene variants, blood serum level with the susceptibility to CRC. (springeropen.com)
  • The gene NPM1 that encodes for nucleophosmin (NPMI) is translocated or mutated in various lymphomas and leukemias, forming fusion proteins (NPM-ALK, NPM-RARa, NPM-MLF1) or NPM mutant products. (haematologica.org)
  • 4 Nucleophosmin is an essential protein, since inactivation of the gene encoding for nucleophosmin ( NPM1 ) in the mouse germ line leads to developmental defects that cause embryonic death in mid-gestation. (haematologica.org)
  • It is also associated with the regulation of APOPTOSIS and microtubule assembly. (nih.gov)
  • A variety of malignancies including hepatocellular carcinoma (HCC) show de-regulation of nuclear transport factors such as overexpression of the exportin Cellular Apoptosis Susceptibility (CAS). (oncotarget.com)
  • By analyzing ~ 1700 proteins using quantitative mass spectrometry in HCC cells we found that CAS depletion by RNA i leads to de-regulation of integrins, particularly down-regulation of integrin β1. (oncotarget.com)
  • In contrast, intracellular NAMPT is involved in nicotinamide mononucleotide synthesis and has been implicated in the regulation of cellular apoptosis, although the exact mechanisms for this regulation are poorly understood. (nih.gov)
  • Inhibition of nicotinamide mononucleotide synthesis by FK866 (a selective NAMPT enzymatic inhibitor) failed to alter TNF-α-induced human lung EC apoptosis, suggesting that NAMPT-dependent NAD+ generation is unlikely to be involved in regulation of TNF-α-induced EC apoptosis. (nih.gov)
  • Interacting with various cellular proteins, E6 and E7 influence fundamental cellular functions like cell cycle regulation, telomere maintenance, susceptibility to apoptosis, intercellular adhesion and regulation of immune responses. (bijuterii-anca.ro)
  • Our data suggest that TJ regulation, intestinal barrier function and apoptosis are regulated by a ROCK dependent, caveolin-1 mediated pathway. (hhs.gov)
  • More recently, and in collaboration with researchers from national and international institutions, I have been using yeast as an ¿in vivo¿ system for functional and molecular studies of individual mammalian apoptotic regulators, such as proteins of the Bcl-2 family and of their regulation. (cienciavitae.pt)
  • I am currently investigating the regulation of Bax-dependent cell death by N-terminal acetylation as well as the mechanisms underlying the anti-tumoral activity of the milk protein lactoferrin and the signaling pathways involved in acetic acid/acetate-induced cell death. (cienciavitae.pt)
  • PTPN2 is also highly expressed in human and murine beta cells and it has been shown to be critical for beta cell function in vivo and inhibit inflammatory stimuli-mediated beta cell apoptosis in vitro, suggesting that PTPN2 mediated defense against inflammation is two pronged negative regulation of inflammatory immune cells and elevation of a beta cell intrinsic defense. (columbia.edu)
  • RAG1 expressed from this construct lacked an epitope tag to avoid potential tag-associated artefacts that could alter RAG protein localization, regulation, or activity. (vegfr-1inhibitor.com)
  • This review summarizes the innate and adaptive effectors that contribute to susceptibility, immune control and pathogenesis of HSV, and highlights the delicate interplay between these two important arms of immunity. (mdpi.com)
  • Although we have made progress understanding the effect of maternal colonization patterns on neonatal sepsis, there is a gap in the understanding of the regulatory processes that regulate intestinal barrier function that contribute to susceptibility to sepsis. (hhs.gov)
  • Under apoptotic stimulation, GSK-3β was activated after Akt was inactivated and GSK-3β was inhibited-either pharmacologically or using short hairpin RNA to abolish galectin-3, increase apoptosis, and inhibit colony formation-which suggests a pro-survival role for GSK-3β. (tmu.edu.tw)
  • We show in this article that small molecule antagonists of the sigma-1 receptor inhibit tumor cell survival to reveal caspase-dependent apoptosis. (hw.ac.uk)
  • Results shown above support the following conclusions: (a) Ras protein mediates O2(-) radical generation through reduction of molecular oxygen by NADPH oxidase in Cr(VI)-stimulated cells. (cdc.gov)
  • Transfer RNAs (tRNA) have long been believed an evolutionary-conserved molecular family, which play the key roles in the process of protein biosynthesis in plant life activities. (bvsalud.org)
  • The use of intestinal organoids generated from human infants and from ROCK and caveolin-1 knockout mice, will provide tremendous translational power and allow us to probe epithelial functions at molecular, cellular, tissue, and organismal levels. (hhs.gov)
  • Main scientific area of research/Other scientific areas Cellular and Molecular Biology/ Regulated Cell Death in yeast and mammalian cell lines Currently my main scientific research area is on Regulated Cell Death and on the use of yeast as a cellular model to study the biochemical/molecular mechanisms underlying this process. (cienciavitae.pt)
  • 65 genomic loci associated with susceptibility to type 2 diabetes, but little progress has been made in elucidating the molecular mechanisms behind most of these associations. (diabetesjournals.org)
  • We offer a selection of recent papers on a variety of topics from the Journal of Biological Chemistry , the Journal of Lipid Research and Molecular & Cellular Proteomics . (asbmb.org)
  • In a new paper in the journal Molecular & Cellular Proteomics , researchers at the Instituto Tecnologico de Chascomus in Buenos Aires and the University of California, Los Angeles, enriched palmitoylated proteins from T. vaginalis and found numerous palmitoylation sites in pathogenesis-related proteins. (asbmb.org)
  • Along with this correlation, in the absence of the CAS protein in a cell, there is an inhibition of apoptosis Along with being an inducer of apoptosis, CAS also plays a role in being a checkpoint for cell cycle. (wikipedia.org)
  • Novel Mechanism for Nicotinamide Phosphoribosyltransferase Inhibition of TNF-α-mediated Apoptosis in Human Lung Endothelial Cells. (nih.gov)
  • We found that Rho-associated protein kinase (ROCK) is activated during NEC, and inhibition of ROCK confers protection against intestinal barrier injury and disruption of normal TJ homeostasis. (hhs.gov)
  • We will test this hypothesis by determining whether inhibition of TJ protein expression and redistribution or caveolin-1-mediated endocytosis prevent paracellular permeability increases, mucosal and systemic inflammatory responses, and epithelial cell death in experimental sepsis and NEC. (hhs.gov)
  • Collectively, my studies have expanded the understanding of beta cell-specific factors that regulate cellular defense to insulitis and may have expanded the therapeutic possibilities by implicating PKM2, inhibition of which is the focus of many cancer therapy research. (columbia.edu)
  • MicroRNAs (miRNAs) are a newly discovered type of small non-protein coding RNAs (21-25nt) that function in the inhibition of effective mRNA translation through imperfectly base pairing with the 3' untranslated region (3'-UTR) of target mRNAs. (biomedcentral.com)
  • For example, excessive inhibition by which tissue remodeling takes place during normal of apoptosis is an underlying mechanism of cancer, while growth and development and the physiologic mechanism an inappropriate increase is seen in some neurodegenera- by which labile cell populations such as gastrointestinal tive diseases and other conditions. (cdc.gov)
  • Activation of NF-kB prevents apoptosis in response to the tumor necrosis factor family of cytokines. (medscape.com)
  • Cells that retain IKK activity may produce additional cytokines that trigger apoptosis in neighboring IKK-deficient cells, thus creating an amplification loop that eventually results in the death of all of the IKK-deficient cells. (medscape.com)
  • Two recent genome-wide association studies (GWASs) [ 9 , 10 ] indicated associations between single nucleotide polymorphisms (SNPs) of the major histocompatibility complex (MHC) class I region, some cytokines, and BD susceptibility. (molvis.org)
  • Rho kinases (ROCK) are serine/ threonine kinases and are involved in multiple cellular processes including regulating tight junction function, actin cytoskeleton contraction, inflammatory cytokines and cell death. (hhs.gov)
  • They measured histopathological damage, the levels of proinflammatory cytokines, and reactive oxygen species in kidney tissues and apoptosis ratio. (hindawi.com)
  • Research opportunities include identifying mechanisms of cellular injury and survival, understanding genetic factors influencing susceptibility, and identifying pharmacologic avenues for protection and rescue from NIHL. (nih.gov)
  • Our findings indicate that the aged brain has the capability to mount a cytoproliferative response to injury, but the timing of the cellular and genetic response to cerebral insult is dysregulated in aged animals, thereby further compromising functional recovery. (nih.gov)
  • In recent years, it has become evident that the traditional central dogma of DNA transcription into messenger RNA (mRNA) and mRNA translation into proteins describes only a part of the genetic information machinery that determines which proteins might possibly be synthesized. (biomedcentral.com)
  • Additional genetic information is required to control the timing and rates of protein manufacturing processes. (biomedcentral.com)
  • 3. Genetic Determinants of Susceptibility to Environmental Agents. (elsevier.com)
  • Modeling genetic susceptibility to cancer in the mouse. (elsevier.com)
  • Insulin resistance which develops from obesity and physical inactivity acts as substrate for genetic susceptibility [ 10 ]. (hindawi.com)
  • Prevention of lymphocyte apoptosis, same process by which these cell populations are regulat- through either genetic modification of the host or treatment ed during normal health ( 1 , 2 ). (cdc.gov)
  • The present study investigate the mechanisms by which O2(-) radical mediates signals from Ras protein to the nucleus, leading to cellular responses such as apoptosis in Cr(VI)-stimulated cells. (cdc.gov)
  • Compared to Ras(-) cells, Ras(+) cells exhibited higher susceptibility to apoptosis induced by Cr(VI). (cdc.gov)
  • Galectin-3 expression was time- and transcription-dependently deregulated in K562 chronic myeloid leukemia cells stimulated for apoptosis by cisplatin (a platinum-based chemotherapy drug), sphingolipid ceramide analog C2-ceramide, and LY294002 (a phosphatidylinositol 3-kinase inhibitor). (tmu.edu.tw)
  • We found that GSK-3β upregulated galectin-3 and stabilized anti-apoptotic Bcl-2 family proteins, which is important for the escape of leukemia cells from apoptotic stimuli. (tmu.edu.tw)
  • Separation of the Hexokinase II from the VDAC pore on the outer mitochondrial membrane triggers apoptosis (programmed cell death) of the cancer cell while sparing normal cells. (greenmedinfo.com)
  • 3BP (3 Bromo Pyruvate) is a small non-toxic molecule that induces apoptosis in cancer cells while sparing normal cells, thus providing the most promising cancer treatment we have seen in many years. (greenmedinfo.com)
  • Thankfully, there are many other compounds in the natural world that act on this same mechanism of selectively inducing apoptosis in cancer cells while sparing normal cells. (greenmedinfo.com)
  • In particular, the lysosomal protease Cathepsin D was shown to play a similar role in acetate-induced apoptosis in colorectal cancer cells as its orthologue Pep4p in acetic acid-induced apoptosis in yeast cells. (cienciavitae.pt)
  • Here, we used a global proteomic approach based on high-resolution mass spectrometry to compare the extracellular and intracellular roles of IL-33 in primary human endothelial cells, a major source of IL-33 protein in human tissues. (nature.com)
  • We found that exogenous extracellular IL-33 cytokine induced expression of a distinct set of proteins associated with inflammatory responses in endothelial cells. (nature.com)
  • Full length IL-33 is biologically active and it can be released from the nucleus of producing cells after cellular damage or necrotic cell death 26 , 27 . (nature.com)
  • During inflammation, IL-33 is processed in the central activation domain by inflammatory proteases from mast cells and neutrophils, that generate mature forms of the protein with 10 to 30 fold higher biological activity 29 , 30 . (nature.com)
  • To identify novel candidates that function in the beta cells to influence beta cell susceptibility to insulitic injury, I established RNA transcriptome and CpG dinucleotide methylome profiles of islets isolated from insulitis susceptible NOD and insulitis resistant NOR mice, prior to the onset of insulitis. (columbia.edu)
  • In a paper in the Journal of Lipid Research , Zhenzhen Zhang and colleagues at Northwest A&F University in Shaanxi, China, reported that in a model for apoptosis in fat cells, two microRNAs are important drivers of the programmed cell death pathway. (asbmb.org)
  • Expressed in human umbilical vein endothelial cells (HUVECs) (at protein level) (PubMed:19342684, PubMed:17580308). (affbiotech.com)
  • Isoform Delta15 is expressed in brain, testis, ovary, cell surface of platelets, human umbilical vein endothelial cells (HUVECs), Jurkat T-cell leukemia, human erythroleukemia (HEL) and U-937 histiocytic lymphoma cell lines (at protein level) (PubMed:12433657, PubMed:18388311). (affbiotech.com)
  • Knocking down expression of Na + /K + -ATPase, the cellular receptor of cardenolides, in ST cells was found to significantly impair the susceptibility of ST cells to TGEV infectivity. (researcher-app.com)
  • Extensive lymphocyte severe infections is a massive loss of lymphocytes, den- apoptosis has also occurred in humans and animals infect- dritic cells, gastrointestial epithelial cells, and other cell ed with several exotic agents, including Bacillus anthracis , types through apoptosis, or programmed cell death. (cdc.gov)
  • Under native conditions, both in resting and proliferating cells, over 95% of cellular NPM protein exists as an oligomer. (haematologica.org)
  • The homozygous TT genotypes and T variant allele of IGF-1 rs6214(C/T) showed association with high serum Insulin growth factor level 1, may increase susceptibility to the colorectal cancer. (springeropen.com)
  • To date, about 50 IDDM susceptibility loci have been mapped to specific chromosome regions in the human. (biomedcentral.com)
  • For example, the apparatus governing the cell cycle is able to modulate cell differentiation [ 40 ] and programmed cell death (apoptosis). (medscape.com)
  • A functional insertion/deletion polymorphism in the promoter of PDCD6IP is associated with the susceptibility of hepatocellular carcinoma in a Chinese population. (cdc.gov)
  • Thus, studies of alcohol's effects on t he structure and function of cellular organelles are critical to better understand the mechanisms of alcohol-induced injuries and to develop new strategies for their diagnosis and treatment. (nih.gov)
  • These interactions are considered critical for at least some normal functions of alpha-synuclein, and may well play critical roles in both the aggregation of the protein and its mechanisms of toxicity. (en-journal.org)
  • Understanding the mechanisms of beta cell-intrinsic factors that influence the maintenance of cellular defenses and contribute to cell death when deregulated will be crucial in efforts to treat or prevent beta cell loss in individuals who are prone to autoimmunity. (columbia.edu)
  • The results of our meta-analysis suggest that TNF (−308A/G, −238A/G, −1031C/T, and −857T/C) polymorphisms are associated with susceptibility to BD. (molvis.org)
  • Roles of functional NFKB1 and ß-TrCP insertion/deletion polymorphisms in mRNA expression and epithelial ovarian cancer susceptibility. (cdc.gov)
  • Since new DNA must be packaged into nucleosomes to function properly, synthesis of canonical (non-variant) histone proteins occurs alongside DNA replication. (wikipedia.org)
  • The authors review among others mice with a knockout of proteins involved in ER folding machinery, UPR signaling, degradation of aggregated proteins, and protein trafficking and secretion. (hindawi.com)
  • The cellular apoptosis susceptibility (CSE1L/CAS) protein is a microtubule-associated protein that is highly expressed in cancer. (tmu.edu.tw)
  • CSE1L-GFP (green fluorescence protein) fusion protein experiments showed that the N-terminal of CSE1L interacted with microtubules. (tmu.edu.tw)
  • Chromosome segregation 1-like (CSE1L), also called cellular apoptosis susceptibility protein (CAS), is highly expressed in breast cancer and plays a crucial role in the progression of various tumours. (bvsalud.org)
  • The cellular apoptosis susceptibility protein (CAS) is an exportin which in the nucleus is bound to RanGTP. (wikipedia.org)
  • In addition, the process of DC activation and maturation is accompanied by the production of exosomes, which are cell‑derived extracellular vesicles (EVs) that can carry proteins, lipids, nucleic acids, and other cargoes involved in intercellular communication and material transfer. (spandidos-publications.com)
  • Drs Ko and Pederson discovered a small molecule called 3BP which throws a "monkey wrench" into the metabolic machinery of the cancer cell, and induces apoptosis via separation of Hexokinase II from the outer mitochondrial membrane. (greenmedinfo.com)
  • Interestingly, this upregulation of amino-acid transporters, as well as increased L-leucine/L-isoleucine metabolism, is found in GlcN-exposed liver specimen of rodents, thereby suggesting that the glycolytic inhibitor GlcN induces a metabolic switch towards increased protein metabolism in both worms and mice, unambiguously culminating in extended life span. (anti-agingfirewalls.com)
  • 10. Expression of TGF-beta 1 protein and mRNA and the effect on the tissue remodeling in laryngeal carcinomas. (nih.gov)
  • The authors report the increased susceptibility of an aged kidney to ER stress with excessive reactive oxygen species level using a mouse model. (hindawi.com)
  • Here we show that GlcN, independent of the hexosamine pathway, extends Caenorhabditis elegans life span by impairing glucose metabolism that activates AMP-activated protein kinase (AMPK/AAK-2) and increases mitochondrial biogenesis. (anti-agingfirewalls.com)
  • Protein misfolding in the ER triggers the activation of three homologous transmembrane protein kinases, Ire1, the PKR-like ER kinase (PERK), and the transmembrane transcription factor ATF6. (hindawi.com)
  • Mitogen-Activated Protein Kinase (MAPK) signal transduction pathways regulated by stresses and toxicants. (elsevier.com)
  • The Cas family of proteins can be divided into 4 functional domains: expression, interference, adaption, and ancillary. (wikipedia.org)
  • This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS. (reference.md)
  • Manual 26.29 HN - 2002 MH - Activin Receptors UI - D029404 MN - D8.586.913.696.620.682.700.62 MN - D12.776.543.750.750.400.820.500 MS - Receptors for ACTIVINS are membrane protein kinases belonging to the family of PROTEIN-SERINE-THREONINE KINASES, thus also named activin receptor-like kinases (ALK's). (nih.gov)
  • The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (oncotarget.com)
  • Pathways involved in unfolded protein response are important for normal cellular homeostasis and organismal development and may also play key roles in the pathogenesis of many diseases. (hindawi.com)
  • A single-amino-acid substitution in the TvbS1 receptor results in decreased susceptibility to infection by avian sarcoma and leukosis virus subgroups B and D and resistance to infection by subgroup E in vitro and in vivo. (omia.org)
  • Cell cycle arrest was able to preserve a non-activated cellular phenotype through prevention of adhesion molecule expression in vivo , thereby reducing the susceptibility to atherosclerosis or vasculopathy. (medscape.com)
  • to use fluorescent proteins for in vivo monitoring of cellular processes in Saccharomyces cerevisiae, and in the determination of yeast antifungal susceptibility. (cienciavitae.pt)
  • In contrast, overexpression of NAMPT served to reduce degrees of TNF-α-induced EC apoptosis. (nih.gov)
  • [ 41 ] Furthermore, VSMC is inhibited when cell cycle progression is blocked by overexpression of the cell cycle-inhibitory protein p21 CIP1 or antisense oligonucleotides (ODNs) against c- myc . (medscape.com)
  • Apoptotic stimuli decreased pro-survival Bcl-2 family protein expression (especially Mcl-1), whereas galectin-3 overexpression reversed but it was enhanced by a galectin-3 expression knockdown. (tmu.edu.tw)
  • Nicotinamide phosphoribosyltransferase (NAMPT) exists as both intracellular NAMPT and extracellular NAMPT (eNAMPT) proteins. (nih.gov)
  • Exosomes are cell-derived, nm-sized extracellular vesicles (EVs) that are formed through the endocytosis and inward budding of the endosomal membrane mediated by extracellular components and cell surface proteins. (spandidos-publications.com)
  • Galectin-3 is regulated for cancer cell survival and apoptosis depending upon the cell type and stimulus. (tmu.edu.tw)
  • Resistance to the B subgroup of avian sarcoma and leukosis viruses is a single-locus trait, with susceptibility being dominant and resistance recessive (Crittenden et al. (omia.org)
  • Forced galectin-3 expression caused resistance to apoptosis, whereas knockdown galectin-3 expression increased susceptibility to apoptosis. (tmu.edu.tw)
  • The acquisition of resistance to apoptosis, the cell's intrinsic suicide program, is essential for cancers to arise and progress and is a major reason behind treatment failures. (hw.ac.uk)
  • Cellular organelles play an important role in cellular functions and are significantly involved in alcohol-induced tissue injury. (nih.gov)
  • Oxidative stress plays a pivotal role in cellular injury from hyperglycemia. (hindawi.com)
  • 14 B23.1, the prevalent isoform in all tissues, 15 contains 294 amino acids, 16 whereas B23.2, a truncated protein, lacks the last 35 C-terminal amino acids of B23.1 and is expressed at very low levels. (haematologica.org)
  • 3. None of your MAGs have been associated for the biosynthesis or acquisition of compati ble solutes such as glycine betaine, and there was no evi dence that any proteins have excessive quantities of acidic amino acids or hydrophobic residues, suggesting they don't accumulate intracellular salts as being a mechanism of osmoregulation. (thrombin-inhibitor.com)
  • This Funding Opportunity Announcement (FOA) issued by the National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, encourage s Research Project Grant (R01) applications that propose to study biological processes involving the cellular organelles in alcohol-induced tissue injury. (nih.gov)
  • Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are only recently coming to light. (nih.gov)
  • Endoplasmic reticulum (ER) stress triggers complex adaptive or proapoptotic signaling defined as the unfolded protein response (UPR), involved in several pathophysiological processes. (hindawi.com)
  • We next confirmed that TNF-α-induced EC apoptosis is attributable to NAMPT secretion into the EC culture media and subsequent eNAMPT ligation of TLR4 on the EC membrane surface. (nih.gov)
  • The apoptotic subfamily can be further divided into initiator caspases, which are activated in response to death signals, and executioner caspases, which are activated by the initiator caspases and are responsible for cleavage of cellular substrates that ultimately lead to cell death. (thermofisher.com)
  • Catalase, sodium formate, and deferoxamine inhibited Cr(VI)-induced apoptosis. (cdc.gov)
  • The review further examines the main toxic effects of ROS on lipid, protein, glutathione metabolism, catalase, superoxide dismutases, and antioxidant capacity of plasma. (hindawi.com)
  • Caspase 7 is an executioner caspase that was identified based on its homology with caspases 1 and 3, as well as the C. elegans cell death protein CED-3. (thermofisher.com)
  • To do this, we studied the expression of proliferating cell nuclear antigen (PCNA) by immunostaining and at apoptosis by in situ nick end-labeling (TUNEL), followed by calculation of the PCNA labeling index (PCNA LI) and TUNEL labeling index (TUNEL LI). (nih.gov)
  • An early cellular response to DNA damage is increased expression of the p53 protein. (nih.gov)
  • We examined the role of NAMPT in TNF-α-induced human lung endothelial cell (EC) apoptosis and demonstrated that reduced NAMPT expression (siRNA) increases EC susceptibility to TNF-α-induced apoptosis as reflected by PARP-1 cleavage and caspase-3 activation. (nih.gov)
  • Because the skin metastases originating from breast and lung can express the p63 protein, the use of this expression remains controversial and so, further investigations are mandatory. (asspub.ro)
  • Furthermore, the expression of plasticity-associated proteins, such as MAP1B, was delayed in aged rats. (nih.gov)
  • Cellular susceptibility appears to correlate with differences in sigma receptor coupling rather than levels of expression. (hw.ac.uk)
  • Human papillomavirus infection mice, Human papillomavirus infection mice - Hpv virus en herpes Human Human papillomavirus and mice - HPV - Nucleus Health what causes papilloma in throat Human papillomavirus infection mice cara menghilangkan kutil papilloma, cervical warts removal paraziti v lidskem tele lecba. (alexandrudiaconescu.ro)
  • Rimedi naturali per ossiuri nei bambini hhh Cervical Cancer Oral Sex - Human papilloma virus in male Papiloma en la boca de mi perro Implicarea genomului papiloma virusului uman hpv în oncogeneza cancerului cervical Human papilloma virus strains Schistosomiasis schistosomiasis guatemala guatemala guatemala to some recent studies, the HPV infection may also increase the risk of cardiovascular diseases. (zppp.ro)
  • This work establishes the importance of palmitoylation in T. vaginalis proteins for infection and suggests that palmitoylation enzyme inhibitors may help treat the infection. (asbmb.org)
  • Lymphocytes, in particular, undergo massive and infection, potentially improving outcomes for patients in a apparently unregulated apoptosis in human patients and variety of disease states. (cdc.gov)
  • Apoptosis is a specialized sequence of events that a cell can induce for programmed death. (wikipedia.org)
  • This special issue intends to address the different aspects relating interaction between oxidative stress, UPR, and cellular redox capacity. (hindawi.com)
  • They found that the ER stress in the kidney is a consequence of sepsis and it is connected with oxidative stress and the ER stress-related apoptosis. (hindawi.com)
  • The early infarct in older rats is associated with a premature accumulation of BrdU-positive microglia and astrocytes, persistence of activated oligodendrocytes, a high incidence of neuronal degeneration, and accelerated apoptosis. (nih.gov)
  • Alpha-synuclein is a small neuronal protein that is closely associated with the etiology of Parkinson's disease. (en-journal.org)
  • These results indicate that there is an augmentation of pro-liferative activity and apoptosis in HCC tissue, as compared to non-tumor tissue. (nih.gov)
  • Tissue recovery was further delayed by the upregulation of Nogo, ephrin-A5 and MAG, which exert a powerful negative effect on axonal sprouting in the aged peri-infarct cortex, and by an age-related increase in the amount of the neurotoxic C-terminal fragment of the beta-amyloid precursor protein (betaAPP) at 2 wks post-stroke. (nih.gov)
  • In other parasites, a protein modification called palmitoylation, the addition of a 16-carbon saturated fatty acid to cysteine residues of a protein, regulates infectivity. (asbmb.org)
  • Human papillomavirus HPV - Early Vaccination paraziti v jatrech Dysbiosis gut hpv wart virus symptoms, papiloma en perros en la boca tratamiento hpv warts child. (bijuterii-anca.ro)
  • Human papillomavirus yleisyys hpv virus en zwanger willen worden, juvenile papilloma virus metastatic cancer kya hota h. (wishstudio.ro)
  • Although only a minority of the human genome (2-3%) codes for proteins, a large fraction of the non-protein coding genome is transcribed. (biomedcentral.com)
  • To date there is no direct evidence linking miRNAs and human T1D susceptibility. (biomedcentral.com)
  • Susceptibility of p53-deficient mice to induction of mesothelioma by crocidolite asbestos fibers. (nih.gov)
  • Instead of polyadenylated tails , canonical histone transcripts possess a conserved 3` stem loop motif that selective binds to Stem Loop Binding Protein ( SLBP ). (wikipedia.org)
  • 20 Through its N-terminal hydrophobic domain, NPM also exerts a chaperone activity, preventing protein aggregation in the nucleolus, favoring histone and nucleosome assembly, 21 - 23 and increasing acetylation-dependent transcriptional activity. (haematologica.org)
  • The N-terminal ~100 residues of the protein constitute a lipid-binding domain that contains 7 imperfect 11-residue repeats, each centered on a variation of a KTKEGV core consensus sequence. (en-journal.org)
  • A nucleocytoplasmic transport protein that binds to ALPHA KARYOPHERINS and RAN GTP BINDING PROTEIN inside the CELL NUCLEUS and participates in their export into CYTOPLASM . (nih.gov)
  • Although alpha-synuclein is a highly soluble, cytoplasmic protein, it binds to a variety of cellular membranes of different properties and compositions. (en-journal.org)
  • Here we review the known features of alpha-synuclein membrane interactions in the context of both the putative functions of the protein and of its pathological roles in disease. (en-journal.org)

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