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๋ฌธ์„œ ๊ฒ€์ƒ‰์„ ์œ„ํ•œ ๋„์›€์ด ํ•„์š”ํ•˜์‹ ๊ฐ€์š”?
  • Mapping the spatio-temporal pattern of the mammalian target of rapamycin (mTOR) activation in temporal lobe epilepsy. 22761730

    Growing evidence from rodent models of temporal lobe epilepsy (TLE) indicates that dysregulation of the mammalian target of rapamycin (mTOR) pathway is involved in seizures and epileptogenesis. However, the role of the mTOR pathway in the epileptogenic process remains poorly understood. Here, we used an animal model of TLE and sclerotic hippocampus from patients with refractory TLE to determine whether cell-type specific activation of mTOR signaling occurs during each stage of epileptogenesis. In the TLE mouse model, we found that hyperactivation of the mTOR pathway is present in distinct hippocampal subfields at three different stages after kainate-induced seizures, and occurs in neurons of the granular and pyramidal cell layers, in reactive astrocytes, and in dispersed granule cells, respectively. In agreement with the findings in TLE mice, upregulated mTOR was observed in the sclerotic hippocampus of TLE patients. All sclerotic hippocampus (n = 13) exhibited widespread reactive astrocytes with overactivated mTOR, some of which invaded the dispersed granular layer. Moreover, two sclerotic hippocampus exhibited mTOR activation in some of the granule cells, which was accompanied by cell body hypertrophy. Taken together, our results indicate that mTOR activation is most prominent in reactive astrocytes in both an animal model of TLE and the sclerotic hippocampus from patients with drug resistant TLE.
    ๋ฌธ์„œ ํƒ€์ž…:
    Reference
    ์นดํƒˆ๋กœ๊ทธ ๋ฒˆํ˜ธ:
    MAB377
    ์ œํ’ˆ๋ช…:
    Anti-NeuN Antibody, clone A60
  • The long noncoding RNA MALAT1 regulates the lipopolysaccharide-induced inflammatory response through its interaction with NF-ฮบB. 27434861

    MALAT1 is a conserved long noncoding RNA whose expression correlates with many human cancers. However, its significance in immunity remains largely unknown. Here, we observe that MALAT1 is upregulated in lipopolysaccharide (LPS)-activated macrophages. Knockdown of MALAT1 increases LPS-induced expression of TNFฮฑ and IL-6. Mechanistically, MALAT1 was found to interact with NF-ฮบB in the nucleus, thus inhibiting its DNA binding activity and consequently decreasing the production of inflammatory cytokines. Additionally, abnormal expression of MALAT1 was found to be NF-ฮบB-dependent. These findings suggest that MALAT1 may function as an autonegative feedback regulator of NF-ฮบB to help fine-tune innate immune responses.
    ๋ฌธ์„œ ํƒ€์ž…:
    Reference
    ์นดํƒˆ๋กœ๊ทธ ๋ฒˆํ˜ธ:
    17-700
    ์ œํ’ˆ๋ช…:
    Magna RIPโ„ข RNA-Binding Protein Immunoprecipitation Kit
  • The retinoblastoma protein regulates pericentric heterochromatin. 16612004

    The retinoblastoma protein (pRb) has been proposed to regulate cell cycle progression in part through its ability to interact with enzymes that modify histone tails and create a repressed chromatin structure. We created a mutation in the murine Rb1 gene that disrupted pRb's ability to interact with these enzymes to determine if it affected cell cycle control. Here, we show that loss of this interaction slows progression through mitosis and causes aneuploidy. Our experiments reveal that while the LXCXE binding site mutation does not disrupt pRb's interaction with the Suv4-20h histone methyltransferases, it dramatically reduces H4-K20 trimethylation in pericentric heterochromatin. Disruption of heterochromatin structure in this chromosomal region leads to centromere fusions, chromosome missegregation, and genomic instability. These results demonstrate the surprising finding that pRb uses the LXCXE binding cleft to control chromatin structure for the regulation of events beyond the G(1)-to-S-phase transition.
    ๋ฌธ์„œ ํƒ€์ž…:
    Reference
    ์นดํƒˆ๋กœ๊ทธ ๋ฒˆํ˜ธ:
    Multiple
    ์ œํ’ˆ๋ช…:
    Multiple
  • The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway. 27740626

    Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are of great importance in different cell contexts. However, only a very small number of lncRNAs have been experimentally validated and functionally annotated during human hematopoiesis. Here, we report an lncRNA, HOTAIRM1, which is associated with myeloid differentiation and has pivotal roles in the degradation of oncoprotein PML-RARA and in myeloid cell differentiation by regulating autophagy pathways. We first revealed that HOTAIRM1 has different variants that are expressed at different levels in cells and that the expression pattern of HOTAIRM1 is closely related to that of the PML-RARA oncoprotein in acute promyelocytic leukemia (APL) patients. We further revealed that the downregulation of HOTAIRM1 could inhibit all-trans retinoic acid (ATRA) -induced degradation of PML-RARA in APL cells and repress the process of differentiation from promyelocytic to granulocytic cells. More importantly, we found that HOTAIRM1 regulates autophagy and that autophagosome formation was inhibited when HOTAIRM1 expression was reduced in the cells. Finally, through the use of a dual luciferase activity assay, AGO2 RNA immunoprecipitation and RNA pull-down, HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2. We constructed a human APL-ascites SCID mouse model to validate the function of HOTAIRM1 and its regulatory pathway in vivo. This is the first report showing that a lncRNAs regulates autophagy and the degradation of the PML-RARA oncoprotein during the process of myeloid cell differentiation blockade, suggesting that lncRNAs may be the potential therapeutic targets for leukemia.
    ๋ฌธ์„œ ํƒ€์ž…:
    Reference
    ์นดํƒˆ๋กœ๊ทธ ๋ฒˆํ˜ธ:
    17-700
    ์ œํ’ˆ๋ช…:
    Magna RIPโ„ข RNA-Binding Protein Immunoprecipitation Kit
  • The type 1 insulin-like growth factor receptor and resistance to DACH1. 21558809

    The mammalian homolog of the Drosophila dachshund gene (DACH1) has been reported as a tumor suppressor in human breast and prostate cancers. It downregulates the epidermal growth factor receptor (EGFR) and cyclin D1. The signaling pathway of the type 1 insulin-like growth factor receptor (IGF-IR) is known to be responsible for the development of resistance to treatment of human cancer with antibodies to the EGFR. We have asked whether DACH1 still exerts its tumor suppressor activity in cells dependent on the IGF-IR for growth. We find that in cells growing in IGF-1 (and unresponsive to EGF), DACH1 is devoid of tumor suppressor activity.
    ๋ฌธ์„œ ํƒ€์ž…:
    Reference
    ์นดํƒˆ๋กœ๊ทธ ๋ฒˆํ˜ธ:
    06-248
    ์ œํ’ˆ๋ช…:
    Anti-IRS1 Antibody
  • The physical state of the LDL core influences the conformation of apolipoprotein B-100 on the lipoprotein surface. 12505152

    We assessed the influence of temperature on the secondary structure of apolipoprotein B-100 (apoB) in normal low-density lipoprotein (N-LDL) and triglyceride-rich LDL (T-LDL). Gradual heating from 7 degrees C to the phase-transition temperature of the lipoprotein core ( approximately 28 degrees C and approximately 15 degrees C for N-LDL and T-LDL, respectively) gradually altered the secondary structure of apoB, while further heating from the phase-transition temperature to 45 degrees C had no additional effect. Above the phase-transition temperature of the core, the apoBs of N-LDL and T-LDL had a similar secondary structure. These results indicate that the conformation of apoB on the LDL surface depends strongly on the physical state of the lipoprotein core, and less on the lipid composition of the core per se.
    ๋ฌธ์„œ ํƒ€์ž…:
    Reference
    ์นดํƒˆ๋กœ๊ทธ ๋ฒˆํ˜ธ:
    AB3395
  • The bromodomain protein Brd4 insulates chromatin from DNA damage signalling. 23728299

    DNA damage activates a signalling network that blocks cell-cycle progression, recruits DNA repair factors and/or triggers senescence or programmed cell death. Alterations in chromatin structure are implicated in the initiation and propagation of the DNA damage response. Here we further investigate the role of chromatin structure in the DNA damage response by monitoring ionizing-radiation-induced signalling and response events with a high-content multiplex RNA-mediated interference screen of chromatin-modifying and -interacting genes. We discover that an isoform of Brd4, a bromodomain and extra-terminal (BET) family member, functions as an endogenous inhibitor of DNA damage response signalling by recruiting the condensin II chromatin remodelling complex to acetylated histones through bromodomain interactions. Loss of this isoform results in relaxed chromatin structure, rapid cell-cycle checkpoint recovery and enhanced survival after irradiation, whereas functional gain of this isoform compacted chromatin, attenuated DNA damage response signalling and enhanced radiation-induced lethality. These data implicate Brd4, previously known for its role in transcriptional control, as an insulator of chromatin that can modulate the signalling response to DNA damage.
    ๋ฌธ์„œ ํƒ€์ž…:
    Reference
    ์นดํƒˆ๋กœ๊ทธ ๋ฒˆํ˜ธ:
    Multiple
    ์ œํ’ˆ๋ช…:
    Multiple