Nam Kim

Crif1 is a novel transcriptional coactivator of STAT3

Signal transducer and activator of transcription 3 (STAT3) is a transcriptional factor that performs a broad spectrum of biological functions in response to various stimuli. However, no specific coactivator that regulates the transcriptional activity of STAT3 has been identified. Here we report that CR6‐interacting factor 1 (Crif1) is a specific transcriptional coactivator of STAT3, but not of STAT1 or STAT5a. Crif1 interacts with STAT3 and positively regulates its transcriptional activity. Crif1−/− embryos were lethal around embryonic day 6.5, and manifested developmental arrest accompanied with defective proliferation and massive apoptosis. The expression of STAT3 target genes was markedly reduced in a Crif1−/− blastocyst culture and in Oncostatin M‐stimulated Crif1‐deficient MEFs. Importantly, the key activities of constitutively active STAT3‐C, such as transcription, DNA binding, and cellular transformation, were abolished in the Crif1‐null MEFs, suggesting the essential role of Crif1 in the transcriptional activity of STAT3. Our results reveal that Crif1 is a novel and essential transcriptional coactivator of STAT3 that modulates its DNA binding ability, and shed light on the regulation of oncogenic STAT3.

Mind bomb-1 is an essential modulator of long-term memory and synaptic plasticity via the Notch signaling pathway

BackgroundNotch signaling is well recognized as a key regulator of the neuronal fate during embryonic development, but its function in the adult brain is still largely unknown. Mind bomb-1 (Mib1) is an essential positive regulator in the Notch pathway, acting non-autonomously in the signal-sending cells. Therefore, genetic ablation of Mib1 in mature neuron would give valuable insight to understand the cell-to-cell interaction between neurons via Notch signaling for their proper function.ResultsHere we show that the inactivation of Mib1 in mature neurons in forebrain results in impaired hippocampal dependent spatial memory and contextual fear memory. Consistently, hippocampal slices from Mib1-deficient mice show impaired late-phase, but not early-phase, long-term potentiation and long-term depression without change in basal synaptic transmission at SC-CA1 synapses.ConclusionsThese data suggest that Mib1-mediated Notch signaling is essential for long-lasting synaptic plasticity and memory formation in the rodent hippocampus.

Survival and Differentiation of Mammary Epithelial Cells in Mammary Gland Development Require Nuclear Retention of Id2 Due to RANK Signaling

ABSTRACT RANKL plays an essential role in mammary gland development during pregnancy. However, the molecular mechanism by which RANK signaling leads to mammary gland development is largely unknown. We report here that RANKL stimulation induces phosphorylation of Id2 at serine 5, which leads to nuclear retention of Id2. In lactating Id2Tg; RANKL−/− mice, Id2 was not phosphorylated and was localized in the cytoplasm. In addition, in lactating Id2S5ATg mice, Id2S5A (with serine 5 mutated to alanine) was exclusively localized in the cytoplasm of mammary epithelial cells (MECs), while endogenous Id2 was localized in the nucleus. Intriguingly, nuclear expression of Id2S5A rescued increased apoptosis and defective differentiation of MECs in RANKL−/− mice. Our results demonstrate that nuclear retention of Id2 due to RANK signaling plays a decisive role in the survival and differentiation of MECs during mammary gland development.

The resistance anomaly in the surface layer of Bi2Sr2CaCu2O8+x single crystals under radio-frequency irradiation

Abstract We observed that radio-frequency (rf) irradiation significantly enhances the c -axis resistance near and below the superconducting transition of the CuO 2 layer in contact with a normal-metal electrode on the surface of Bi 2 Sr 2 CaCu 2 O 8+ x single crystals. We attribute the resistance anomaly to the rf-induced charge imbalance nonequilibrium effect in the surface CuO 2 layer. The relaxation of the charge-imbalance in this highly anisotropic system is impeded by the slow quasiparticle recombination rate, which results in the observed excessive resistance.

Resistance enhancement of the intrinsic surface junction of Bi2Sr2CaCu2O8+x single crystal under radio-frequency irradiation

Abstract It is found that radio-frequency irradiation significantly enhances the c-axis resistance near the superconducting transition of the CuO2 bi-layer located on the surface of a Bi2Sr2CaCu2O8+x single crystal. The features of this resistance anomaly are similar to those observed recently in the mesoscopic aluminum wires and structutes with normal-metal/superconductor interfaces, where the resistance anomaly is caused by the nonequilibrium charge-imbalance effect.

Quantum transport in ultrathin CoSi2 polycrystalline films

Abstract Quantum transport in ultrathin CoSi 2 polycrystalline films was studied for the first time. The temperature corrections to the conductivity of these films and their anomalous magnetoresistance have been observed and investigated. It is shown that they are determined by the effects of interaction and weak localization with the strong spin-orbit and spin scattering taken into account. Unlike the epitaxial crystalline films reported previously our films including one with the thickness larger than 10 nm show no superconductivity down to the lowest temperature (0.2 K). In the thinnest film we used an unusual dimensional crossover from one dimensional behavior of quantum corrections to two dimensional have been observed with lowering temperature, supposedly due to changes of the characteristic correlation length in the sample, which consisted of meandrous conducting paths caused by the presence of pin-holes.

Quasiparticle conduction in mesoscopic wires containing N-S-N junctions

We measured the dynamic resistance (dV/dI) of mesoscopic normal-metal/superconductor/normal-metal (N-S-N) junctions. At low temperatures (T<4 K), we observed dips indV/dI at zero bias and anomalous peaks near the bias of 2ΔPbln/e (where 2ΔPbln is the gap energy of superconducting Pb-In) and at higher biasVc The zero-bias dips are supposed to originate from Andreev reflections of electrons and the peaks near 2ΔPbln/e from the interference of quasiparticles inside S. We attribute the peaks atVc to the transition of the superconducting region to the normal state as the current exceeds the critical currentIc of S.