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At least 1,657 records · Page 92Linked to original sources
PubMed1998

Accumulation of IL-12-activated antitumor effector cells into lymph nodes of tumor-bearing mice.

Simultaneous administration of high dose of IL-12 into tumor-inoculated mice resulted in a marked reduction of tumor growth in parallel with the augmented generation of cytotoxic T-cells, natural killer (NK) cells and IFN-gamma-producing Th cells. We found that these IL-12-activated antitumor effector cells preferentially accumulated in peripheral lymph nodes concomitantly with lymphadenopathy. However, IL-12 rather induced disappearance of antitumor effector cells including CD4+ T, CD8+ T and NK cells from spleen in spite of inducing splenomegaly. Lymph node cells obtained from IL-12-treated B16F0-bearing mice showed a marked IFN-gamma production in response to not only IL-2, IL-12, anti CD3 mAb but also B16F0 melanoma cells. Moreover, they could lyse B16F0 melanoma cells in a long-term cytotoxicity assay. It was also confirmed that IL-12-activated IFN-gamma producing Th1 cells were accumulated in tumor local site. Thus, IL-12 appeared to have a capability of stimulating selective migration of antitumor cells into lymph nodes and tumor local sites.

Animals↗
PubMed1999

In vivo acquired mechanisms of tumor cells local defense against the host innate immunity effectors: implication in specific antitumor immunity.

As shown earlier, the cells transformed in vitro by several different oncogenes, or spontaneously, during in vivo growth in normal hosts would be gradually replaced by the highly-tumorigenic descendants co-expressing high H2O2-catabolizing and PGE2-releasing activities. Acquisition of (H2O2(CA) + PGE(S)) phenotype provides the cells with local defense mechanisms against the host innate immunity effectors. However, it remained unknown, whether the expression of (H2O2(CA) + PGE(S)) phenotype is implicated in susceptibility of tumor cells expressing tumor-specific transplantation antigens to rejection in immune animals. Here, with the use of SV40 in vitro transformed parental cells, negative in expression (H2O2(CA) + PGE(S)) phenotype, and their in vivo selected descendant tumor cell lines expressing this phenotype, we show that: (1) the rates of in vivo selection of the parental SV40 tumor cells expressing (H2O2(CA) + PGE(S)) phenotype are the same in normal and SV40-immune animals; (2) in vivo selected SV40 tumor cells expressing (H2O2(CA) + PGE(S)) phenotype, although they retain specific immunosensitivity, are 100 times less effectively rejected in SV40-immunized animals, as compared with their in vitro SV40-transformed parental cells. Thus, in vivo acquired immunologically non-specific local mechanisms of tumor cells defense against the host innate immunity effectors, significantly decreases the effectiveness of their specific immunorejection.

Animals↗
PubMed2002

Chemokine receptor expression on MBP-reactive T cells: CXCR6 is a marker of IFNgamma-producing effector cells.

Cytokine-polarized T cells have distinct chemokine receptor (CKR) expression patterns associated with their cytokine secretion profiles. In order to investigate this paradigm in autoreactive human T cells, we have determined the CKR expression pattern of myelin basic protein (MBP)-reactive T cell lines (TCL) and compared these profiles to those of TCL-generated in response to tetanus toxoid (TT). Expression of CXCR6 and CXCR3 on TCL was significantly positively correlated with IFNgamma, and inversely correlated with IL-5 production. TT TCL had significantly higher expression of CCR7(-)/CD45RA(-) T effector memory (Tem) cells than MBP TCL. However, in MBP-specific TCL, CXCR6 was found to be the best marker of conversion to the Tem phenotype. CXCR6 and CXCR3 are likely to be important in the migration of effector memory T cells in Th1-mediated inflammatory diseases such as multiple sclerosis (MS).

Biomarkers↗
PubMed2003

Kinetics of CCR7 expression differ between primary activation and effector memory states of T(H)1 and T(H)2 cells.

We explored the kinetics of CCR7 expression on T(H)1 and T(H)2 polarized cells as well as on antigen-specific T cell lines at various stages of differentiation. A striking pattern of early (days 7-14) inducible CCR7 expression was seen preferentially on primary T(H)1 cell lines, as compared to T(H)2 cells, and was dependent on the strength and duration of the T cell receptor signal. Upon repeated restimulation (days 21-28) and differentiation, a switch occurred in which T(H)2 cells had high CCR7 expression, whereas T(H)1 cells lost CCR7 expression. Chronic (8 weeks and later) effector memory cell lines were 95% CCR7 negative. These data demonstrate an ordered pattern of CCR7 expression that suggest more rapid priming of T(H)1 cells in the lymph node, and delayed priming with prolonged CCR7 expression during T(H)2 responses, and may have implications for tracking T(H)1 effector T cells ex vivo in autoimmune diseases.

Antigen Presentation↗
PubMed1997

Degenerate antigen recognition by CD4+ effector T cells in experimental autoimmune encephalomyelitis.

Peptide-specific tolerance with PLP139-151 peptide analogs was used to compare the fine antigen-specificity requirements at both the inductive and effector phases of relapsing EAE (R-EAE). A PLP139-151 analog peptide containing a single substitution at the primary T cell receptor (TcR) contact residue (A144) did not induce proliferation in PLP139-151-primed CD4+ T cells. In addition, tolerance induced with ECDI-treated. A144-coupled splenocytes failed to prevent the inductive phase of PLP139-151-induced R-EAE or to inhibit the induction of peptide-specific DTH indicating that naive PLP139-151-specific T cells do not react with the A144 peptide analog. In contrast, A144-coupled splenocytes did prevent the expression of the effector phase of R-EAE and inhibited the elicitation of peptide-specific DTH responses upon administration to mice seven days after immunization with PLP139-151. The results provide in vivo evidence that "antigen-experienced' T cells recognize a broader repertoire of antigens than do naive T cells and have important implications for the regulation of immune responses and for advancing our understanding of the pathogenesis and treatment of autoimmune disease.

Amino Acid Sequence↗
PubMed1999

Sensing effectors make sense.

'Housekeepers' of living organisms maintain salt and water balance, monitor blood sugar and schedule their work to the season and the time of day. In order to perform their chores, they rely on information about the status quo. The traditional concept of a sensor that communicates with a central comparator authorizing an effector, which was inspired by engineers, has become blurred in the search for morphological correlates of such regulatory cascades. In many cases, neurones, which are both sensory and neurosecretory, and endocrine cells equipped with smart detectors, reliably regulate autonomous functions by using local rather than central computing. Like the well-trained staff of a smoothly run household, such 'sensing effectors' translate information into action.

Animals↗
PubMed2000

Novel allosteric effectors of the tryptophan synthase alpha(2)beta(2) complex identified by computer-assisted molecular modeling.

Tryptophan synthase is a pyridoxal 5'-phosphate-dependent alpha(2)beta(2) complex catalyzing the formation of L-tryptophan. The functional properties of one subunit are allosterically regulated by ligands of the other subunit. Molecules tailored for binding to the alpha-active site were designed using as a starting model the three-dimensional structure of the complex between the enzyme from Salmonella typhimurium and the substrate analog indole-3-propanol phosphate. On the basis of molecular dynamics simulations, indole-3-acetyl-X, where X is glycine, alanine, valine and aspartate, and a few other structurally related compounds were found to be good candidates for ligands of the alpha-subunit. The binding of the designed compounds to the alpha-active site was evaluated by measuring the inhibition of the alpha-reaction of the enzyme from Salmonella typhimurium. The inhibition constants were found to vary between 0.3 and 1.7 mM. These alpha-subunit ligands do not bind to the beta-subunit, as indicated by the absence of effects on the rate of the beta-reaction in the isolated beta(2) dimer. A small inhibitory effect on the activity of the alpha(2)beta(2) complex was caused by indole-3-acetyl-glycine and indole-3-acetyl-aspartate whereas a small stimulatory effect was caused by indole-3-acetamide. Furthermore, indole-3-acetyl-glycine, indole-3-acetyl-aspartate and indole-3-acetamide perturb the equilibrium of the catalytic intermediates formed at the beta-active site, stabilizing the alpha-aminoacrylate Schiff base. These results indicate that (i) indole-3-acetyl-glycine, indole-3-acetyl-aspartate and indole-3-acetamide bind to the alpha-subunit and act as allosteric effectors whereas indole-3-acetyl-valine and indole-3-acetyl-alanine only bind to the alpha-subunit, and (ii) the terminal phosphate present in the already known allosteric effectors of tryptophan synthase is not strictly required for the transmission of regulatory signals.

Allosteric Regulation↗
PubMed2000

Investigation of the role of the carboxyl-terminal tails of the alpha and beta isoforms of the human thromboxane A(2) receptor (TP) in mediating receptor:effector coupling.

We have investigated the functional coupling of alpha and beta isoforms of the human thromboxane A(2) receptor (TP) to Galpha(16) and Galpha(12) members of the G(q) and G(12) families of heterotrimeric G proteins in human embryonic kidney (HEK) 293 cell lines HEK.alpha10 or HEK.beta3, stably over-expressing TPalpha and TPbeta, respectively. Moreover, using HEK.TP(Delta328) cells which over-express a variant of TP truncated at the point of divergence of TPalpha and TPbeta, we investigated the requirement of the C-tail per se in mediating G protein coupling and effector activation. Both TPalpha and TPbeta couple similarly to Galpha(16) to affect increases in inositol 1,4,5-trisphosphate (IP(3)) and mobilisation of intracellular calcium ([Ca(2+)](i)) in response to the TP agonist U46619. Whilst both TP isoforms mediated [Ca(2+)](i) mobilisation in cells co-transfected with Galpha(12), neither receptor generated corresponding increases in IP(3), indicating that the Galpha(12)-mediated increases in [Ca(2+)](i) do not involve PLC activation. Verapamil, an inhibitor of voltage dependent Ca(2+) channels, reduced [Ca(2+)](i) mobilisation in TPalpha and TPbeta cells co-transfected with Galpha(12) to approximately 40% of that mobilised in its absence, whereas [8-(N,N-diethylamino)-octyl-3,4, 5-trimethoxybenzoate, hydrochloride] (TMB-8), an antagonist of intracellular Ca(2+) release, had no effect on [Ca(2+)](i) mobilisation by either receptor isoform co-transfected with Galpha(12). Despite the lack of differential coupling specificity by TPalpha and TPbeta, TP(Delta328) signalled more efficiently in the absence of a co-transfected G protein compared to the wild type receptors but, on the other hand, displayed an impaired ability to couple to co-transfected Galpha(11), Galpha(12) or Galpha(16) subunits. In studies investigating the role of the C-tail in influencing coupling to the effector adenylyl cyclase, similar to TPalpha but not TPbeta, TP(Delta328) coupled to Galpha(s), leading to increased adenosine 3',5'-cyclic monophosphate (cAMP), rather than to Galpha(i). Whereas TP(Delta328) signalled more efficiently in the absence of co-transfected G protein compared to the wild type TPalpha, co-transfection of Galpha(s) did not augment cAMP generation by TP(Delta328). Hence, from these studies involving the wild type TPalpha, TPbeta and TP(Delta328), we conclude that the C-tail sequences of TP are not a major determinant of G protein coupling specificity to Galpha(11) and Galpha(16) members of the G(q) family or to Galpha(12); it may play a role in determining G(s) versus G(i) coupling and may act as a determinant of coupling efficiency.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1998

Limiting dilution analysis of peripheral blood lymphocytes reacting with non-small-cell lung cancer: functionally heterogeneous effectors efficiently lyse autologous cancer cells.

It has recently been shown that the infusion of tumor infiltrating lymphocytes (TIL) and recombinant interleukin-2 (rIL-2) in patients operated on for advanced non-small-cell lung cancer (NSCLC), has significant effects in terms of the survival time and control of local relapses. Despite the evident clinical effects, the treatment is unavailable for patients in which TIL have lost their proliferative potential. In an attempt to identify new sources of effector cells using mixed lymphocyte/tumor cultures (MLTC), populations of peripheral blood (PB) lymphoid cells, which have the capability of lysing autologous NSCLC, were studied at the clonal level. Specific cytolytic lymphocytes were detected at very low frequencies in two out of four patients, whereas non-MHC restricted cytolytic T cells were frequently detected. Cytolytic CD4+ belonged to the Th0 or Th2 subsets and were characterized by cytokine secretion patterns suggestive of a lymphokine cascade that could be involved in cancer control. The identification of different efficient effector mechanisms at the clonal level strongly supports the use of in vitro activated lymphocytes, derived from PB, in protocols of adoptive immunotherapy in patients with advanced NSCLC in which TIL are unavailable.

Aged↗
PubMed1990

Thymic stromal cells induce hapten-specific, genetically restricted effector suppressor cells in vivo.

Thymic stromal cells (TSC) from CKB (H-2k) and B10.BR (H-2k) mice were cultured to examine if these cell populations would induce suppressor cell responses. I-A molecules were not detected on the surface of TSC, however, following incubation of these cells with recombinant interferon (IFN)-gamma, I-A antigens were induced. Non-specific esterase activity was seen in 5% of the cultured B10.BR cells but was absent in CKB derived cultures. Morphologically, both CKB and BR-TSC populations lacked an epithelial ultrastructure and cytokeratin immunoreactivity, hence were mesenchymal. As there was no evidence of surface Mac-1 and 33D1 molecules, these cells were not of macrophage or dendritic cell lineage. Both B10.BR and CKB TSC cells (1 x 10(4] induced effector suppressor cells when chemically conjugated with the hapten, NP-O-Succinamide (NP) and injected subcutaneously into syngeneic mice. The suppression by transferred lymph node cells was not always present when TSC were cultured in medium without IFN-gamma, but after incubation with IFN-gamma for 4 days, a significant suppression was consistently evident. Genetically restricted induction of suppressive activity was noted when the I-J-congenic strains of mice, B10.A (5R) and B10.A (3R), were used as the lymph node donors; suppressor cells generated in 5R (I-Jk) mice, significantly suppressed the syngeneic response, whereas in the 3R (I-Jb) strain, there was no significant suppression. The suppression was hapten-specific and depended on both the number of TSC and the dose of IFN-gamma. All these data taken together suggest that, although the TSC used in this study appears to be a mixture of heterogeneous cell populations from the thymic stroma, TSC are capable of inducing hapten-specific, genetically restricted effector suppressor cells when IFN-gamma is included in the culture system.

Animals↗
PubMed1981

Effector cell sensitivity to sugar moieties. I. Inhibition of human natural killer cell activity by monosaccharides.

Human natural killer (NK) cells recognize multiple target antigens. The ligands (antigens) involved in the effector-target cell interaction have not been extensively identified. In the present study, assays of NK activity in the presence of a panel of monosaccharides demonstrated inhibition of cytolysis in a dose-response fashion. We propose that NK cell activity involves the recognition of carbohydrate structures on target cells via receptors on the effector cell surface.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1983

Target-effector-cell interactions in the human natural-killer(NK)-system: isolation of target structures.

The existence of structures on NK-sensitive target cells selectively recognized by the effector cells have been postulated. To test this hypothesis, four selected human cell lines were investigated for target-cell proteins which could serve as specific ligands for the putative NK-cell receptor(s). NP-40 extracts from two highly NK-sensitive (K 562 and Molt-4) and two rather insensitive cell lines (HL-60 and Reh-6) were fractionated on SDS-polyacrylamide gels and tested for their ability to inhibit binding of effector to target cells as well as NK cytotoxicity. Three fractions with molecular weights (MW) of 200, 120 and 80 +/- 10 KD isolated from K 562 cells were able to inhibit binding of large granular lymphocytes (LGL) to K 562. Of the other cell lines, Molt-4 and HL-60, both which were able to inhibit lysis of K 562 in a cold target inhibition assay, showed also two inhibitory fractions with MW 120 and 80 KD, whereas Reh-6, which is not able to compete with 51Cr-labelled K 562 in a cytotoxicity assay, lacked these structures. The 200, 120 and 80 KD fractions isolated from K 562 and the 120 and 80 KD fractions from Molt-4 and HL-60 were able to inhibit lysis of K 562 cells when added to the cytotoxicity assay. By adsorption/elution of radiolabelled K 562 extracts to/from LGL it was possible to detect an 80 KD target-cell surface protein which became preferentially bound by LGL-enriched but not by LGL-depleted lymphocyte preparations. Our results indicate the existence of target-cell proteins in NK-sensitive cell lines which serve as specific ligands for binding of NK cells. These target-cell structures of human cell lines differed from NK target structures described for mouse-NK-sensitive cell lines.

Binding, Competitive↗
PubMed1988

Delayed type hypersensitivity (DTH) in anti-IgM-treated B cell-depleted mice: analysis of induction and effector phase.

The induction and the effector phase of murine delayed type hypersensitivity (DTH) were evaluated in mice treated from birth with anti-IgM antibodies; these mice had no mature B cells and could not produce an antibody response. To study the effector phase, long-term cultured cloned helper T cells were injected subcutaneously together with the specific antigen into the hind footpad of normal and B cell-deficient mice. Antigen-specific DTH responses assessed by the local swelling reaction 24 h after transfer measured against a particulate antigen (sheep red blood cells, SRBC) as well as a soluble antigen (ovalbumin, OVA) were unaffected by the absence of B cells. To study the induction phase of DTH, 3-day immune in vivo primed lymphocytes from normal or B cell-depleted mice were adoptively transferred by subcutaneous injection into the hind footpad of naive syngeneic recipients. B cell depletion did not affect the induction of cells capable of responding to SRBC; in contrast, the response to soluble antigen (OVA) was significantly reduced, suggesting that B cells or their products participated in the induction of a DTH response to a soluble antigen.

Animals↗
PubMed2002

beta-cell antigen-specific CD56(+) NKT cells from type 1 diabetic patients: autoaggressive effector T cells damage human CD56(+) beta cells by HLA-restricted and non-HLA-restricted pathways.

Studies of type 1 diabetes indicate that autoaggressive T cells specific to beta-cell antigens, reaching certain threshold levels, may play critical roles in the development of the disease. Flow cytometric analyses found that autoreactive T-cell lines from patients induced by beta-cell antigens consisted of four major subsets (CD4(+)CD56(-), CD4(+)CD56(+), CD8(+)CD56(-), and CD8(+)CD56(+)) and that CD56(+) NKT cells might be derived from CD56(-) T cells. Moreover, the proportion of CD56(+) NKT cells in the T-cell lines was influenced by time course of repeated antigen stimulation. beta-cell antigen-specific CD56(+) NKT (CD4(+) or CD8(+)) cells were more aggressive (HLA-restricted and -unrestricted) effector cells lysing target cells such as K562, Jurkat, P815 plus anti-CD3 antibody, and autologous B cells sensitized by beta-cell peptides, when compared with their CD56(-) counterparts. beta-cell antigen- specific CD4(+)CD56(+) NKT cells showed non-HLA-restricted cytotoxicity to human beta cells, insulinoma cell line CM, and to islet cell lines TRM-6 and HP62 expressing CD56 but not to four CD56(-) pancreatic cell lines of non- islet origin. The CD4(+)CD56(+) NKT cells showed stronger cytotoxicity to CM, TRM-6 and HP62 cells than did CD4(+)CD56(-) T cells. Moreover, isotope-unlabelled CD56(+) cells and anti-CD56 antibodies were able to inhibit cytotoxicity of CD4(+)CD56(+) NKT to CD56(+) target cells. These results suggest that CD56(+) NKT cells are aggressive cytotoxic cells to beta cells and that CD56 expression might be associated with the aggressiveness of effector T cells and the susceptibility of target cells.

Adolescent↗
PubMed2001

Effector cytotoxic T lymphocyte numbers induced by vaccination should exceed levels in chronic infection for protection from HIV.

Recent technological advances have revolutionised our capacity to induce cytotoxic T lymphocyte (CTL) responses with a variety of vaccine formulations and delivery systems. However, the conditions required for a CTL-inducing vaccine to provide protection from infection or disease are poorly understood, and the results of challenge experiments have not been consistent. Here we use a mathematical model to examine the requirements necessary for successful vaccination against human immunodeficiency virus (HIV) through cellular immunity. We describe the interaction between cytotoxic T cells and infected lymphocytes, capturing the essence of a persistent infection of immune cells. We conclude that to protect from infection, the cellular immune response should be boosted to levels exceeding those in chronic infection. This requires either that effector CTL exceed this threshold before infection, or that a memory CTL population is established that can yield this level of effector CTL very quickly upon infection.

AIDS Vaccines↗
PubMed1975

[Comparative metabolism of phospholipids of osmoregulation effector organs in European eel (Anguilla anguilla)].

The phospholipid composition from various organs of the fresh water eel, such as gill, kidney, gut, liver and muscle, were determined by thin-layer chromatography. The major phosphatides found in these tissues were PC, PE and SPH and minor constituents PS, PI, DPG, AP and also LPC in the gut. A greater percentage of PS and SPH occurs in the osmoregulatory effector organs such as gill, kidney, and gut. From in vivo comparative kinetic studies of the 32P incorporation into the phospholipids, between 6 and 48 hours, certain remarkable features of phospholipid metabolism have been found in these tissues. A low uptake of inorganic 32P into the tissue lipid phosphorus was observed in the eel at 15 degrees C. The specific activity of the lipid phosphorus increased continuously in all tissues during 48 hours after 32P injection. During this experimental period, phosphatidic acid and phosphatidyl inositol fractions were labelled most rapidly in gill, kidney and gut, while the specific activity of the phosphatidyl choline fraction remained low in these organs. In liver, the rate of PC formation appears to be faster than the PI and PE biosynthesis. In gill and gut, the PE showed greater turnover than the PC as measured by 32P incorporation. In the eel, an euryhalin fish, the DPG of osmoregulatory effector organs has a high specific activity at all times. PS showed only a high specific activity in the gill. Labelling of SPH occured slowly in the various tissues only becoming evident after 24 hours. The results are compared with those published for other poikilotherm and homeotherm vertebrates. Relative differences between the turnover of various tissue phosphatides are discussed with of reference to the general scheme on phospholipid biosynthesis and to the physiological functions of the various organs.

Anguilla↗
PubMedDate not supplied

Insulin regulation of protein phosphorylation in hepatocytes. Studies using two effectors: amiloride and natural aliphatic polyamines.

The effects of amiloride and of natural aliphatic polyamines on basal and hormone-stimulated protein phosphorylations in hepatocytes were studied. Cells isolated from adult rats were incubated in suspension with (32P)-orthophosphate, in the absence or presence of the effectors at varying concentrations and for different times; hepatocytes were then exposed to various hormones for 10 min. Phosphoproteins contained in total cell lysates were analyzed by one- and two-dimensional gel electrophoresis and autoradiography. Amiloride and spermine (the most effective amine) decreased the basal level of phosphorylation of proteins of 46, 34 and 22 kDal, and increased that of 18 kDal and 93 kDal proteins. These effects were maximal with external concentrations of 1 mM and 7.5-10 mM amiloride and spermine, respectively. They were detectable after a lag period of about 10 min and reached a plateau after 45 min. Pretreatment of cells with these effectors almost completely prevented stimulation of the phosphorylation of the 46 and 34 kDal proteins by insulin. In contrast, the effects of vasopressin on the same proteins were only partly inhibited, whereas those of glucagon appeared largely unaffected. The major effect observed in intact cells (i.e., decreased phosphorylation) could be reproduced in a cell-free system where no kinase activity persisted. Amiloride or spermine added directly to cell extracts strongly accelerated the dephosphorylation of 46 kDal protein and also of the 61 kDal protein identified as pyruvate kinase. Furthermore, restoration of the activity of this enzyme occurred concomitantly with dephosphorylation of the 61 kDal protein, an observation supporting the notion that amiloride and spermine could activate a phosphoprotein phosphatase.

Amiloride↗
PubMed2000

JNK and p38 stresskinases--degenerative effectors of signal-transduction-cascades in the nervous system.

The c-Jun N-terminal kinases (JNKs, also called stress activated protein kinases. SAPKs) and p38 kinases constitute together with extracellular signal-regulated kinases (ERKs) the family of MAP kinases. Whereas the functions of JNKs under physiological conditions are largely unknown, there is raising evidence that JNKs are potent effectors of apoptosis or degeneration of neurons in vitro and in the brain. The activation of the inducible transcription factor c-Jun by N-terminal phosphorylation is a central event in JNK-mediated degenerative processes that depend on de novo protein synthesis. At the post-translational level, cytoplasmic degenerative actions of JNKs might comprise inhibition of Bcl-2 and steroid hormone-receptor signaling or hyperphosphorylation of tau; and at transcriptional level, JNKs might trigger the induction of the apoptotic effectors p53 and Fas-Ligand by phosphorylation of c-Jun. The role of p38 is the nervous system is poorly understood, but its activation is also considered as part of the neuronal stress response. This review informs about the genetic processing, the regulation of activity and the biochemical actions of JNK and p38 isoforms in general. In the second part, we summarize the findings on expression and activation of JNKs and p38 under neurodegenerative condition. A particular focus is also put on the putative function of JNK under physiological conditions and for neuroprotection.

Animals↗