Viewing affirmative mentions of protein catabolism in T cells

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Duprez et al. (1988)IL2T cellWe have described a human tumor T cell line, IARC 301, which constitutively expresses high affinity interleukin 2 (IL2) receptors, and showed that after binding to its receptors, IL2 is endocytosed and degraded.
de Azevedo et al. (2003)PNPT-cellIn human, PNP is the only route for degradation of deoxyguanosine and genetic deficiency of this enzyme leads to profound T-cell mediated immunosuppression.
Isakov et al. (1993)PKCT cellsWe propose that Bryo inhibits PMA-induced T cell proliferation by causing rapid degradation of PKC, reflecting a requirement of persistent PKC stimulation (lasting approximately 48 h) for the activation of human T cells and progression through the cell cycle.
Tanimura et al. (2006)LAT mutantLATThe mouse LAT mutant lacking palmitoylation was unstable and susceptible to degradation via the proteasome pathway.
Ruegg et al. (1992)CD4T lymphocytesDegradation of CD4 following phorbol-induced internalization in human T lymphocytes.
Penna et al. (1999)ZAP-70T lymphocytesDegradation of ZAP-70 following antigenic stimulation in human T lymphocytes: role of calpain proteolytic pathway.
Penna et al. (1999)ZAP-70T cellsTwo lines of evidence indicate that the Ca2+-dependent cysteine protease calpain plays a major role in initiating ZAP-70 degradation: 1) treatment of T cells with cell-permeating inhibitors of calpain markedly reduces ZAP-70 degradation; 2) ZAP-70 is cleaved in vitro by calpain.
Penna et al. (1999)ZAP-70T cellOur results show that, in the course of T cell-APC cognate interaction, ZAP-70 is rapidly degraded via a calpain-dependent mechanism.
Childs et al. (1983)endo-beta-galactosidaseT cellThe O-linked chains are polydisperse and those of B rather than T cell type are highly susceptible to degradation by endo-beta-galactosidase.
Fujii et al. (1986)interleukin 2T cellsHigh-affinity receptor-mediated internalization and degradation of interleukin 2 in human T cells.
Fujii et al. (1986)IL-2T cellReceptor-mediated internalization and degradation of IL-2 were investigated in cell lines carrying human T cell leukemia/lymphoma (lymphotrophic) virus type I (HTLV-I) and PHA-treated normal PBL.
Moore et al. (2001)p27T cellsS phase entry and cell cycle commitment in peripheral T cells requires p27(kip) degradation, normally initiated by the receipt of costimulatory signals such as those provided by B7.1 or IL-2.
Car et al. (1991)CTAP-IIIT-lymphocyteBy contrast, no degradation of CTAP-III was observed with thrombin, plasmin or 'granzymes' from cytolytic T-lymphocyte granules.
Sanfridson et al. (1994)CD4T cellsThe simian immunodeficiency virus Nef protein promotes degradation of CD4 in human T cells.
Santis et al. (1995)CD69 mRNAT lymphocytesWe propose that the selective degradation pathway involved in the regulation of the expression of cytokines and proto-oncogenes is implicated in the rapid degradation of CD69 mRNA in activated T lymphocytes.
Kanno et al. (1995)I kappa B-alphaT cellsTwo I kappa B-alpha mutants defective in extracellular signal-induced degradation of I kappa B-alpha also blocked Tax-mediated kappa B-dependent transactivation when cotransfected into Jurkat T cells.
Barry et al. (1995)CD4T lymphocytesThus, myxoma virus infection of CD4+ T lymphocytes triggers CD4 downregulation via a protein kinase C-independent pathway, causing the dissociation of p56lck and the degradation of CD4 in lysosomal vesicles.
Erbagci et al. (2006)ADAT cellOBJECTIVES: Activity of Serum Adenosine Deaminase (ADA), a main enzyme in purine degradation and considered as a marker for non-specific T cell activation, in psoriasis has been investigated in a few studies with conflicting results.
Bruyns et al. (1995)LPAPT cellsIn CD45-deficient human T cells, LPAP protein is synthesized at normal levels but is more rapidly degraded than in wild-type cells.
de Zoeten et al. (2009)Foxp3T cellsWe show, using retroviral expression of Foxp3 in CD4(+) T cells, that Foxp3 is cleaved at both the N- and C-terminal RXXR sites and that mutagenesis of the RXXR motif prevents cleavage.
Wu et al. (2006)NFATc2T cellsWe show here that NFATc1 and NFATc2 are rapidly degraded in apoptotic T cells.
Ponnappan et al. (2005)IkappaBalphaT lymphocytesConstitutive degradation of IkappaBalpha in human T lymphocytes is mediated by calpain.
Ponnappan et al. (2005)IkappaBalphaT cellsPretreatment with a cell permeable calpain inhibitor, E64D, but not with a proteasome specific inhibitor, lactacystin, blocks stimulus-independent IkappaBalpha degradation in primary human T cells.
Ponnappan et al. (2005)IkappaBalphaT cellsUnlike the previously reported decline in ligand-induced degradation of IkappaBalpha in T cells from the elderly, constitutive degradation does not exhibit an age-associated decline, demonstrating proteasome-independent regulation of the activity.
Ponnappan et al. (2005)IkappaBalphaT cellsCONCLUSION: Our studies support a role for an E64D sensitive protease in regulating constitutive levels of IkappaBalpha in T cells, independent of the involvement of the 26S proteasome, and suggests a biological role for constitutive degradation of IkappaBalpha in T cells.
Cecere et al. (2010)SOD2T cellsOther authors reported that SOD2 is degraded by caspases in Jurkat T cells, following oligomerization of the Fas receptor [20].
Schaecher et al. (2004)IkB alphaT cellThe results suggest that calpain plays an important role in IkB alpha degradation, a crucial event in T cell activation.
Morley and Pain (2001)eIF4GIT cellProteasome inhibitors and immunosuppressive drugs promote the cleavage of eIF4GI and eIF4GII by caspase-8-independent mechanisms in Jurkat T cell lines.
Wu et al. (2006)NFATc1T cellsWe show here that NFATc1 and NFATc2 are rapidly degraded in apoptotic T cells.
Coiras et al. (2008)p65T cellsB transcriptional activity in T cells, the importance of p65/RelA degradation in HIV-1 infected human blood T cells was analyzed.
Schuppler and Loessner (2010)MHC class I moleculesT cellsAlmost any cell type that harbors L. monocytogenes in the cytoplasm can process the proteins secreted from the pathogen, by degradation and subsequent loading on MHC class I molecules, in order to present them on the cell surface to CD8 T cells.
Jiang et al. (2010)endocytic protein antigenT cellsFor example, Ctss is one type of aminothiopropionic acid cathepsin that is mainly expressed in antigen presenting cell participated the positive selection of CD4+ T cells and MHC class II-mediated antigen presentation through both degradation of the endocytic protein antigen and the invariant chain processing pathway [23], [24].
Wernimont et al. (2010)talinT cellsCD4+ and CD8+ T cells developed normally in Capn4F/F:CD4-CRE mice and had severely diminished expression of Calpain 1 and 2, diminished talin proteolysis and impaired casein degradation.
Wernimont et al. (2010)caseinT cellsCD4+ and CD8+ T cells developed normally in Capn4F/F:CD4-CRE mice and had severely diminished expression of Calpain 1 and 2, diminished talin proteolysis and impaired casein degradation.
Chou et al. (2010)UFDT cellsWe have developed a new effective strategy of genetic immunization by activating CD8(+) T cells through the ubiquitin-fusion degradation (UFD) pathway.
de Jong et al. (2010)HIV-1T cellsIn the genital mucosa, two main subsets of DCs are present: epithelial LCs capture and degrade HIV-1 through C-type lectin Langerin, whereas subepithelial DCs express DC-SIGN, which facilitates HIV-1 transmission to T cells.
Wernimont et al. (2010)talinT cellsCD4+ and CD8+ T cells developed normally in Capn4(F/F):CD4-CRE mice and had severely diminished expression of Calpain 1 and 2, diminished talin proteolysis and impaired casein degradation.
Wernimont et al. (2010)caseinT cellsCD4+ and CD8+ T cells developed normally in Capn4(F/F):CD4-CRE mice and had severely diminished expression of Calpain 1 and 2, diminished talin proteolysis and impaired casein degradation.
Hör et al. (2009)T cell receptorT cellFor example the constitutively recycling T cell receptor is ubiquitinated and degraded following receptor stimulation (5).
Serbecic et al. (2009)L-tryptophanT-cellTo conclude, the results of our cell culture experiments and T-cell proliferation assays suggest that the IDO found upregulated in HCECs by stimulation with proinflammatory cytokines is biologically active by degrading L-tryptophan to its key metabolite, L-kynurenine, leading to a suppression of T-cell proliferation and potential cytoprotection in HCEC apoptosis.
Seow et al. (2009)l-tryptophanT-cellsWe then demonstrated that the expressed IDO could catalyse the degradation of l-tryptophan, which in turn suppressed the growth of CD4+ T-cells in a proliferation assay.
Tsuchiyama et al. (2009)fibrinogenT-cellThe maximum CLA+ T-cell percentage was significantly correlated with a high body temperature, low percutaneous oxygen saturation, and fibrinogen/fibrin degradation product D-dimer level.
Tsuchiyama et al. (2009)D-dimerT-cellThe maximum CLA+ T-cell percentage was significantly correlated with a high body temperature, low percutaneous oxygen saturation, and fibrinogen/fibrin degradation product D-dimer level.
Tsuchiyama et al. (2009)fibrinT-cellThe maximum CLA+ T-cell percentage was significantly correlated with a high body temperature, low percutaneous oxygen saturation, and fibrinogen/fibrin degradation product D-dimer level.
Seow et al. (2009)l-tryptophanT-cellsWe then demonstrated that the expressed IDO could catalyse the degradation of l-tryptophan, which in turn suppressed the growth of CD4+ T-cells in a proliferation assay.
Nie et al. (2008)Janus kinasesT-lymphocyteHere, we show that Notch activation accelerates ubiquitin-mediated and mitogen-activated protein kinase (MAPK)-dependent degradation of E2A transcription factors and Janus kinases, molecules essential for both B- and T-lymphocyte development.
Leung et al. (2008)BimELT-cellActivation of the JNK pathway promotes phosphorylation and degradation of BimEL--a novel mechanism of chemoresistance in T-cell acute lymphoblastic leukemia.
Ouchida et al. (2008)CD3zetaT cellA lysosomal protein negatively regulates surface T cell antigen receptor expression by promoting CD3zeta-chain degradation.
Ouchida et al. (2008)CD3zetaT cellThese results identify a lysosomal protein important for CD3zeta degradation and illustrate a unique mechanism for the control of surface TCR expression and T cell activation.
Das et al. (2007)inhibitor IkappaBalphaT cellsLoss in these catalytic activities, following exposure to prooxidant stimulus, also resulted in a decline in both activation-induced proliferation and degradation of the inhibitor IkappaBalpha, with concomitant increase in the accumulation of carbonylated proteins, mimicking responses seen in T cells from the elderly.
Dreolini and Takei (2007)talinT cellsCleavage of talin was undetectable in ionomycin-treated T cells.
El Houda Agueznay et al. (2007)IL-2RalphaT cellsAs MMP-9 has been shown to mediate cleavage of IL-2Ralpha (CD25) by preactivated T cells, we looked for a relationship between MMP-9 expression and soluble IL-2Ralpha serum concentrations in these cancer patients.
Moscarello et al. (2006)myelin protein fragmentsT-cellsDegradation of myelin protein fragments, in particular MBPcit fragments, become available to sensitize T-cells in the periphery, initiating the immune response
Pertovaara et al. (2006)trpT cellIndoleamine 2,3-dioxygenase (IDO), an enzyme involved in the degradation of the essential amino acid tryptophan (trp) to its main metabolite kynurenine (kyn), suppresses T cell activity.
Pertovaara et al. (2006)amino acid tryptophanT cellIndoleamine 2,3-dioxygenase (IDO), an enzyme involved in the degradation of the essential amino acid tryptophan (trp) to its main metabolite kynurenine (kyn), suppresses T cell activity.
Monteleone et al. (2006)MMPsT cellsThe mechanism by which T cells mediate tissue damage during IBD remains unclear, but evidence indicates that T cell-derived cytokines stimulate fibroblasts to synthesise matrix metalloproteinases (MMPs), which then mediate mucosal degradation.
Stepniak et al. (2006)cellT cellMoreover, the A. niger-derived enzyme efficiently degraded all tested T cell stimulatory peptides as well as intact gluten molecules.
Moreno et al. (2006)kappa BT-cellAdministration of MTA suppressed T-cell activation in vivo and in vitro, likely through a blockade in T-cell signaling resulting in the prevention of inhibitor of kappa B (IkappaB-alpha) degradation and in the impaired activation transcription factor nuclear factor-kappaB.
Moreno et al. (2006)IkappaB-alphaT-cellAdministration of MTA suppressed T-cell activation in vivo and in vitro, likely through a blockade in T-cell signaling resulting in the prevention of inhibitor of kappa B (IkappaB-alpha) degradation and in the impaired activation transcription factor nuclear factor-kappaB.
Adam et al. (2005)L-tryptohanT lymphocyteWe were able to demonstrate that IDO mediated degradation of L-tryptohan in HBMEC is responsible for a significant reduction in T lymphocyte proliferation.
Uhlin et al. (2005)zetaT cellHere, we show that T cell receptor triggering results in rapid degradation of the src-family protein kinase lck through a mechanism that is proteasome- and lysosome-independent, sensitive to cysteine protease inhibitors, and distinct from the pathways involved in degradation of ZAP-70 kinase or zeta-chain of the CD3 complex.
Arechiga et al. (2005)IKKT cellsWhereas FADDdd T cells displayed proliferative defects following activation, these were not a consequence of aberrant NF-kappaB signaling, as measured by IKK/IkappaB phosphorylation and IkappaB degradation.
Arechiga et al. (2005)IkappaBT cellsWhereas FADDdd T cells displayed proliferative defects following activation, these were not a consequence of aberrant NF-kappaB signaling, as measured by IKK/IkappaB phosphorylation and IkappaB degradation.
Gould et al. (2004)inducible nitric oxide synthaseT cellsIn vitro studies have shown that doxycycline inhibits bone and cartilage breakdown [37], inhibits matrix metalloproteinases (particularly the activity of matrix metalloproteinase-13 and -8 against CII [38]), increases inducible nitric oxide synthase mRNA degradation [39], and induces Fas/Fas ligand mediated apoptosis of activated T cells [40].
Grundström et al. (2004)cytosolic IkappaBsT cellsImpaired translocation of the p65 subunit in tolerant T cells was a result from reduced activation of IkappaB kinase and poor phosphorylation and degradation of cytosolic IkappaBs.
Cook et al. (2004)HSUR 1T cellsInstead, HSUR 1 itself is degraded by an ARE-dependent pathway in HVS-transformed T cells, suggesting that HVS may take advantage of the host ARE-mediated mRNA decay pathway to regulate HSUR expression.
Zea et al. (2004)CD3zetaT cellThe decreased expression of CD3zeta is not caused by a decreased CD3zeta mRNA, an increased CD3zeta degradation or T cell apoptosis.
Wirleitner et al. (2003)tryptophanT lymphocytesAccording to the cytostatic and antiproliferative properties of tryptophan-depletion on T lymphocytes, activated T-helper type 1 (Th-1) cells may down-regulate immune response via degradation of tryptophan.
He and Ting (2003)I-kappaBalphaT cellsTriggering TCR in mutant Jurkat T cells lacking IKKgamma/NEMO failed to induce IL-2 due to a selective loss in I-kappaB kinase activity, I-kappaBalpha degradation and NF-kappaB DNA-binding activity.
Behbod et al. (2003)TdTT cellsMolecular ablation of Stat5a/b promoted apoptotic cell death in a significant population of primary PHA-activated T cells (72%) and lymphoid tumor cell line (e.g., YT; 74%) within 24 h, as assessed by 1) visualization of karyolytic nuclear degeneration and other generalized cytoarchitectural alterations, 2) enzymatic detection of TdT-positive DNA degradation, and 3) automated cytometric detection of annexin V translocation.
Chowdhury et al. (2003)cellT-cellP53 facilitates degradation of human T-cell leukaemia virus type I Tax-binding protein through a proteasome-dependent pathway.
Robinson and Delvig (2002)protein antigensT cellsMHC class II-restricted antigen presentation to CD4 T cells is achieved by an essentially common pathway that is subject to variation with regard to the location and extent of degradation of protein antigens and the site of peptide binding to MHC class II molecules.
Wieckowski et al. (2002)T-cell receptor zeta chainT-cellGranzyme B-mediated degradation of T-cell receptor zeta chain.
Dumont et al. (2002)CD3T cellsWe studied CD3/TCR down-modulation and zeta degradation in T cells from two ZAP-70-immunodeficient patients.
Hegde et al. (2002)human leukocyte antigenT cellsUS2 also inhibits the MHC-II antigen presentation pathway, causing degradation of human leukocyte antigen (HLA)-DR-alpha and -DM-alpha and preventing recognition by CD4(+) T cells.
Choppin et al. (2001)AgT lymphocytesFirst and foremost among the many factors that influence epitope presentation are the degradation of Ag, which results in peptide liberation, and the presence of HLA class I molecules able to present the peptides to T lymphocytes.
Pessi et al. (2001)caseinT-cellSuppression of T-cell activation by Lactobacillus rhamnosus GG-degraded bovine casein.
Pessi et al. (2001)caseinT-cellGG-degraded bovine casein on T-cell activation, i.e.
Johnson et al. (2001)cellT-cellFree major histocompatibility complex class I heavy chain is preferentially targeted for degradation by human T-cell leukemia/lymphotropic virus type 1 p12(I) protein.
Mukerjee et al. (2001)Cn AT cellTaken together, our results suggest that caspase-mediated cleavage of Cn A contributes to IL-2 production during T cell activation.
Nadano et al. (2001)28S ribosomal RNAT-cellStimulation of death receptors (Fas on human T-cell leukemia Jurkat cells and tumor necrosis factor receptor-1 on human monoblastic leukemia U937 cells) triggers the specific degradation of 28S ribosomal RNA, and this process may contribute to cell death through the inhibition of protein synthesis.
Lee et al. (2000)p27kip1T cellsInterestingly, the kinetics of degradation of p27kip1, a CDK inhibitor, following TCR ligation were faster, and, concomitantly, the up-regulation of CDK2 kinase activity and protein levels were increased in stimulated T cells of STAT1-/- mice relative to those of wild-type mice.
Boussiotis et al. (2000)p27kip1T-cellTherefore, pharmacological agents that upregulate the expression of or prevent the degradation of p27kip1 during antigen recognition should be part of new therapeutic strategies to induce antigen-specific T-cell unresponsiveness.
Khoshnan et al. (2000)I-kappaBalphaT cellsTransduction of proliferating CD4+ T cells with a tetracycline-regulated retrovirus encoding for a dominant-interfering, degradation-resistant I-kappaBalpha (inhibitor of kappa B alpha factor) mutant induced apoptosis.
Yang and Li (2000)XIAPT cellsOur recent studies found the IAP family members XIAP and c-IAP1 are ubiquitinated and degraded in proteasomes in response to apoptotic stimuli in T cells, and their degradation appears to be important for T cells to commit to death.
Machado et al. (2000)I-kappa BT cellsTransformation of T cells by the intracellular parasite Theileria parva is accompanied by constitutive I-kappa B degradation and NF-kappa B activation, a process which is essential to prevent the spontaneous apoptosis of these parasite-transformed cells.
Yu and Kopito (1999)cellT cellThe role of multiubiquitination in dislocation and degradation of the alpha subunit of the T cell antigen receptor.
Uzzo et al. (1999)IkappaBalphaT cellsIn circulating T cells from a subset of patients with RCCs, the suppression of NFkappaB binding activity is downstream from the stimulus-induced degradation of the cytoplasmic factor IkappaBalpha.
Uzzo et al. (1999)IkappaBalphaT cellsTumor-derived soluble products from cultured RCC explants inhibit NFkappaB activity in T cells from healthy volunteers, despite a normal level of stimulus-induced IkappaBalpha degradation in these cells.
Ponnappan (1998)inhibitor I kappa B-alphaT cellSince we have shown that the lowered induction of NF kappa B in activated T cells from the elderly can be attributed to impaired degradation of the inhibitor I kappa B-alpha due to lowered proteasomal activity, we suspect that a similar alteration in proteasomal activity may be operative in age-dependent failure of immune function including the inability to initiate DNA synthesis following activation, skewing of T cell repertoire, lowered cytolytic activity and accumulation of aberrant proteins.
Tortorella et al. (1998)T cell receptor alphaT cellThe T cell receptor alpha (TCR alpha) chain is also degraded by a similar set of reactions, yet in a manner independent of virally encoded gene products.
Sumimoto et al. (1998)class I antigenT cellsIt is unlikely that this is due to cleavage of membranous class I antigen by class I- reactive CD8+ T cells.
Gundersen et al. (1997)tenascin-CT lymphocytePlasmin-induced proteolysis of tenascin-C: modulation by T lymphocyte-derived urokinase-type plasminogen activator and effect on T lymphocyte adhesion, activation, and cell clustering.
Gundersen et al. (1997)plasminT lymphocyteWe have studied the interaction between T lymphocytes and tenascin-C (TN-C), a matrix protein we have previously reported to inhibit T lymphocyte activation, in the context of plasmin-induced degradation.
Gundersen et al. (1997)PlasminT lymphocytesPlasmin proteolysis converts TN-C from a nonadhesive into an adhesive substrate for T lymphocytes and abolishes its aggregating activity on PBMC.
Valitutti et al. (1997)cellT cellDegradation of T cell receptor (TCR)-CD3-zeta complexes after antigenic stimulation.
Matsui et al. (1997)I kappa BT cellOur study integrates the proteasome-dependent I kappa B degradation and NF-kappa B translocation into a T cell activation cascade which results in FasL gene activation and the expression of FasL-mediated cytotoxicity.
Di Modugno et al. (1997)cytoplasmic proteinsCTLsSmall peptides, 8-10 amino acids long, derived from degradation of cytoplasmic proteins by a proteasome-proteinase complex, are usually presented and recognized by CD8+ cytolytic T lymphocytes (CTLs) associated with major histocompatibility complex (MHC) class I molecules.
D'Oro et al. (1997)cellT cellActivation of the Lck tyrosine kinase targets cell surface T cell antigen receptors for lysosomal degradation.