The most intense monitoring observations yet made in the optical and near-infrared wave bands were carried out for Seyfert 1 galaxies NGC 5548, NGC 4051, NGC 3227, and NGC 7469 by the MAGNUM telescope, and clear timedelayed responses of the K-band flux variations to the V-band flux variations were found for all of these galaxies. Their H À K color temperatures of 1500-1800 K, estimated from their observed flux variation gradients, support a view that the bulk of the K flux should originate in the thermal radiation of hot dust surrounding the central engine and that the lag time should correspond to light-travel distance between them. Cross-correlation analysis measures their lag times to be 47-53 (NGC 5548), 11-18 (NGC 4051), about 20 (NGC 3227), and 65-87 (NGC 7469) days. The lag times are tightly correlated with the optical luminosities, as expected from dust reverberation (Át / L 0:5 ), while weakly with the central virial masses, which suggests that the inner radii of the dust tori around active nuclei have oneto-one correspondences with their central luminosities. In the lag time versus central luminosity diagram, the K-band lag times place an upper boundary on the similar lag times of broad emission lines in the literature, which not only supports the unified scheme of AGNs but also implies a physical transition from the BLR out to the dust torus that encircles the BLR. Correlated short-term V-band and X-ray flux variations in NGC 5548 are also found with a delay of 1 or 2 days, indicating the thermal reprocessing of X-ray emission by the central accretion flow.

We present the results of a dust reverberation survey for 17 nearby Seyfert 1 galaxies, which provides the largest homogeneous data collection for the radius of the innermost dust torus. A delayed response of the K-band light curve after the V -band light curve was found for all targets, and 49 measurements of lag times between the flux variation of the dust emission in the K band and that of the optical continuum emission in the V band were obtained by the cross-correlation function analysis and also by an alternative method for estimating the maximum likelihood lag. The lag times strongly correlated with the optical luminosity in the luminosity range of M V = −16 to −22 mag, and the regression analysis was performed to obtain the correlation log ∆t (days) = −2.11 − 0.2M V assuming ∆t ∝ L 0.5 , which was theoretically expected. We discuss the possible origins of the intrinsic scatter of the dust lag-luminosity correlation, which was estimated to be approximately 0.13 dex, and we find that the difference of internal extinction and delayed response of changes in lag times to the flux variations could have partly contributed to intrinsic scatter. However, we could not detect any systematic change of the correlation with the subclass of the Seyfert type or the Eddington ratio. Finally, we compare the dust reverberation radius with the near-infrared interferometric radius of the dust torus and the reverberation radius of broad Balmer emission lines. The interferometric radius in the K band was found to be systematically larger than the dust reverberation radius in the same band by about a factor of two, which could be interpreted by the difference between the flux-weighted radius and the response-weighted radius of the innermost dust torus. The reverberation radius of the broad Balmer emission lines was found to be systematically smaller than the dust reverberation radius by about a factor of 4-5, which strongly supports the unified scheme of the Seyfert type of active galactic nuclei (AGNs). Moreover, we examined the radius-luminosity correlations for the hard X-ray (14-195 keV) and the [O IV]λ25.89 µm emission-line luminosities, which would be applicable for obscured AGNs.

We present new data for five under-luminous type II-plateau supernovae (SNe IIP), namely SN 1999gn, SN 2002gd, SN 2003Z, SN 2004eg and SN 2006ov. This new sample of low-luminosity SNe IIP (LL SNe IIP) is analyzed together with similar objects studied in the past. All of them show a flat light curve plateau lasting about 100 days, an under luminous late-time exponential tail, intrinsic colours that are unusually red, and spectra showing prominent and narrow P-Cygni lines. A velocity of the ejected material below 10 3 km s −1 is inferred from measurements at the end of the plateau. The 56 Ni masses ejected in the explosion are very small ( 10 −2 M ⊙ ). We investigate the correlations among 56 Ni mass, expansion velocity of the ejecta and absolute magnitude in the middle of the plateau, confirming the main findings of Hamuy (2003), according to which events showing brighter plateau and larger expansion velocities are expected to produce more 56 Ni. We propose that these faint objects represent the low luminosity tail of a continuous distribution in parameters space of SNe IIP. The physical properties of the progenitors at the explosion are estimated through the hydrodynamical modeling of the observables for two representative events of this class, namely SN 2005cs and SN 2008in. We find that the majority of LL SNe IIP, and quite possibly all, originate in the core-collapse of intermediate mass stars, in the mass range 10-15 M ⊙ .

Signals emanating from CD40 play crucial roles in B-cell function. To identify molecules that transduce CD40 signalings, we have used the yeast two-hybrid system to clone cDNAs encoding proteins that bind the cytoplasmic tail of CD40. A cDNA encoding a putative signal transducer protein, designated TRAF5, has been molecularly cloned.TRAF5 has a tumor necrosis factor receptor-associated factor (TRAF) domain in its carboxyl terminus and is most homologous to TRAF3, also known as CRAF1, CD40bp, or LAP-1, a previously identified CD40-associated factor. The amino terminus has a RING finger domain, a cluster of zinc fingers and a coiled-coil domain, which are also present in other members of the TRAF family protein except for TRAF1. In vitro binding assays revealed that TRAF5 associates with the cytoplasmic tail of CD40, but not with the cytoplasmic tail of tumor receptor factor receptor type 2, which associates with TRAF2. Based on analysis of the association between TRAF5 and various CD40 mutants, residues 230-269 of CD40 are required for the association with TRAF5. In contrast to TRAF3, overexpression of TRAF5 activates transcription factor nuclear factor #cB. Furthermore, amino-terminally truncated forms ofTRAF5 suppress the CD40-mediated induction of CD23 expression, as is the case with TRAF. These results suggest that TRAF5 and TRAF3 could be involved in both common and distinct signaling pathways emanating from CD40.CD40 is expressed in late B cells in bone marrow, mature B cells, and certain accessory cells, including bone-marrow derived dendritic cells and follicular dendritic cells (1-3), and is a receptor for CD40 ligand (CD40L) present on activated CD4+ T cells (4). Signaling through CD40 rescues B cells from apoptosis induced by crosslinking of the surface immunoglobulin M (IgM) complex (5) and also induces B cells to differentiate and to undergo Ig isotype switching (6, 7). CD40L has been shown to be defective in patients with X-linked hyper IgM syndrome, whose B cells do not form germinal centers and produce only IgM and/or IgD (8). In addition, their B cells have the ability to switch from IgM to IgG, IgE, or IgA production in vitro by the stimulation of CD40 (9). This genetic evidence strongly supports the idea that the intercellular communication through CD40-CD40L is essential for germinal center formation and Ig class switching.CD40 is a member of the tumor necrosis factor receptor (TNFR) superfamily, which includes TNFR1 and TNFR2 (10, 11), lymphotoxin 13 receptor (12), Fas antigen (13), OX40 (14), CD30 (15), and the low-affinity nerve growth factor receptor (16), all of which share a ligand-binding domain composed of tandemly repeated cysteine-rich modules. Among these, Fas antigen and TNFR1 have significant similarity in their cytoplasmic domain over 46 amino acids, a part of the domain called a death domain, suggesting that these receptors could have either common or similar signaling mechanisms (13).Biochemical purification of receptor-associated proteins or the recently developed cDNA...

Accumulative evidence suggests that more than 20 neuron-specific genes are regulated by a transcriptional cis-regulatory element known as the neural restrictive silencer (NRS). A trans-acting repressor that binds the NRS, NRSF [also designated RE1-silencing transcription factor (REST)] has been cloned, but the mechanism by which it represses transcription is unknown. Here we show evidence that NRSF represses transcription of its target genes by recruiting mSin3 and histone deacetylase. Transfection experiments using a series of NRSF deletion constructs revealed the presence of two repression domains, RD-1 and RD-2, within the Nand C-terminal regions, respectively. A yeast two-hybrid screen using the RD-1 region as a bait identified a short form of mSin3B. In vitro pull-down assays and in vivo immunoprecipitation-Western analyses revealed a specific interaction between NRSF-RD1 and mSin3 PAH1-PAH2 domains. Furthermore, NRSF and mSin3 formed a complex with histone deacetylase 1, suggesting that NRSFmediated repression involves histone deacetylation. When the deacetylation of histones was inhibited by tricostatin A in nonneuronal cells, mRNAs encoding several neuronal-specific genes such as SCG10, NMDAR1, and choline acetyltransferase became detectable. These results indicate that NRSF recruits mSin3 and histone deacetylase 1 to silence neural-specific genes and suggest further that repression of histone deacetylation is crucial for transcriptional activation of neural-specific genes during neuronal terminal differentiation.