• Parasites, Hosts and Diseases
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• v.30 no.1
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• pp.33-42
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• 1992

Naegleria fowleri, a free-living amoeba commonly found in moist soil and fresh water, enters the body via the nasal mucosa and migrates along the olfactory nerve to t he brain, where it causes acute amoebic meningoencephalitis. In the present study 7 clones secreting monoclonal antibodies (McAbs) against N. fowleri were produced and the effector function of them was investigated. Their isotopes were IgGl (Nf 1, Nf 154), 19G3 (Nf 137) and 19A (Nf 1, Nf 2, Nf 256, Nf 279). Five McAbs (McAb Nf 2, Nf 279, Nf 27, Nf 154, Nf 137) were specific for N. fowleri by ELISA and recognized the antigenic determinants located on the trophoBoite surface by IFAT and immunoperoxidase stain. These aye McAbs had capacity to agglutinate N. fowleri trophozoites and inhibited the growth of the amoeba in culture medium. McAb Nf 2 inhibited proliferation of trophozoites in vitro significantly. Also the cytotoxicity of JV. fowleri against CHO cell was reduced in the presence of McAb Nf 2 and McAb Nf 154. From these results McAb Nf 2 was confirmed to weaken the virulence of the amoeba among 7 screened McAbs.

• Proceeding of EDISON Challenge
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• 2014.03a
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• pp.225-235
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• 2014

6종의 Intermediate filament 중 type IV인 Neurofilaments (NFs)는 신경세포에 존재하는 세포골격세사로 heavy NF(NF-H), medium NF(NF-M), light NF(NF-L) 세가지의 분자 질량 단백질로 구성되어 있다. NF의 side arm은 interfilament spacing과 axonal caliber를 조절하는 중요한 역할을 한다고 생각되어왔다. 또한 이에 대해서 각각의 protein의 역할은 알아내기 위해 isolated NF의 형태와 구조에 대해 많은 연구가 이루어졌는데, NF의 구조적 특성은 NF sidearm의 tail 부분에서 phosphorylation의 정도에 따른 Lys-Ser-Pro(KSP) repeats의 charge distribution을 통해 알 수 있다. 지금까지 NF에 대한 많은 연구가 이루어졌지만 인간에 한해서만 진행되었다. 그렇기 때문에 본 연구에서는 주어진 amino acid sequence와 각 species의 NF-H:NF-M:NF-L의 비율의 정보를 이용하여 The constant-NVT ensemble MC simulation을 통해 인간뿐만이 아닌 다른 species에 대한 NF의 구조적 특성을 알아보고자 한다.

• Journal of Life Science
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• v.15 no.4 s.71
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• pp.600-606
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• 2005

Neurofilament (NF) proteins constitute the major intermediate filament type in adult neurons. They are made up by the copolymerization of the neurofilament light (NF-L, 61 kDa), medium (NF-M, 90kDa), and heavy (NF-H, 115 kDa) proteins. Although neurofilaments play a crucial .ole in neuronal growth, organization, shape, and plasticity, their expression pattern and cellular distribution in the developing neurons remain unknown. In this study, we have produced a rabbit polyclonal antibody specific to NF-M and investigated expression of NF-M in cultured cortical neurons. Immunostaining of 12 and 24 h cultures revealed strong expression of NF-M in axonal growth cone and in the region of a soma toward the axon. Doublestaining of 4 and 14 DIV corical neurons with NF-M and PSD95 antibodies revealed that both axon and dendrites were stained intensely with NF-M antibody, and that NF-M immunostaining along dendrites is often punctate and colocalize with PSD95 puncta, indicating that the puncta represent postsynaptic spines. Presence of NF-M in the postsynaptic spine was also indicated by immunoblot analysis of the postsynaptic density fraction. Taken together, our results show intensive targeting of NF-M into axons in the early axonal development, and into spines in mature neurons, indicating its important functions in axon and spine development.

• The Journal of Pediatrics of Korean Medicine
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• v.15 no.2
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• pp.69-73
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• 2001

The neurofibromatosis (NF) are a set of genetic disorders which cause tumors to grow along various types of nerves and, in addition, can affect the development of non-nervous tissues such as bones and skin. NF causes tumors to grow anywhere on or in the body. It also leads to developmental abnormalities. For example, individuals with NF have a higher incidence of learning disabilities. Neurofibromatosis(NF) has been classified into two distinct types: NF-I and NF-II. neurofibromatosis 1(NF-I), also known as von Recklinghausen NF or Peripheral NF, occurring in 1:4,000 births, is characterized by multiple cafe-au-lait spots and neurofibromas on or under the skin. Enlargement and deformation of bones and curvature of the spine (scoliosis) may also occur. Occasionally, tumors may develop in the brain, on cranial nerves, or on the spinal cord. About 50% of people with NF also have learning disabilities. Neurofibromatosis 2(NF-II), also known as Bilateral Acoustic NF(BAN), is much rarer occurring in 1:50,000 births. NF-II is characterized by multiple tumors on the cranial and spinal nerves, and by other lesions of the brain and spinal cord. Tumors affecting both of the auditory nerves are the hallmark. Hearing loss beginning in the teens or early twenties is generally the first symptom. We reported a 10-year-old female patient with NF-I, she has pain and edema in left leg, no symptoms of NF.

• Journal of Life Science
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• v.32 no.3
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• pp.241-248
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• 2022

NF-κB acts as a critical transcription factor in inflammation and innate immunity, and it is also closely involved in cell survival and tumorigenesis via induction of anti-apoptotic genes. In these processes, NF-κB cooperates with multiple other signaling molecules and pathways, and although many studies have demonstrated that Hsp90 regulates NF-κB activity, the exact mechanism is unclear. In this study, we investigated the relationship between Hsp90 and IKKγ in the regulation of NF-κB using expression plasmids of IKK complex components. Wild-type and deletion mutants of IKKγ were expressed together with Hsp90, and the combined regulatory effect of Hsp90 and IKKγ on NF-κB activation was assayed. The results show that Hsp90 activates NF-κB by promoting the phosphorylation and degradation of IκBα and that activation of NF-κB by NIK and LPS was increased by Hsp90. IKKγ elevated the effect of Hsp90 on NF-κB activation by increasing phosphorylation and degradation of IκBα. The positive regulation on NF-κB by Hsp90 and IKKγ was also proved in analysis with IKKβ-EE, the constitutively active form of IKKβ. In experiments with the deletion mutants of IKKγ, the N-terminal IKKβ binding domain, C-terminal leucine zipper, and zinc finger domains of IKKγ were found not necessary for the positive regulation of NF-κB activity. Additionally, the expression of pro-inflammatory cytokines was synergistically elevated by Hsp90 and IKKγ. These results indicate that inhibiting the interaction between Hsp90 and IKKγ is a possible strategic method for controlling NF-κB and related diseases.

• Journal of Life Science
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• v.32 no.11
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• pp.833-840
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• 2022

Chronic inflammation has been shown to be closely associated with tumor development and progression. Nuclear factor kappa B (NF-κB) is composed of a family of five transcription factors. NF-κB signaling plays a crucial role in the inflammatory response and is often found to be dysregulated in various types of cancer, making it an attractive target in cancer therapeutics. In this study, CDC-like kinase 3 (CLK3) was identified as a novel kinase that regulates the NF-κB signaling pathway. Our data demonstrate that CLK3 inhibits the canonical and non-canonical NF-κB pathways. Luciferase assays following the transient or stable expression of CLK3 indicated that this kinase inhibited NF-κB activation mediated by Tumor necrosis factor-alpha (TNFα) and Phorbol 12-myristate 13-acetate (PMA), which are known to activate NF-κB signaling via the canonical pathway. Consistent with data on the ectopic expression of CLK3, CLK3 knockdown using shRNA constructs increased NF-κB activity 1.5-fold upon stimulation with TNFα in HEK293 cells compared with the control cells. Additionally, overexpression of CLK3 suppressed the activation of this signaling pathway induced by NF-κB-inducing kinase (NIK) or CD40, which are well-established activators of the non-canonical pathway. To further examine the negative impact of CLK3 on NF-κB signaling, we performed Western blotting following the TNFα treatment to directly identify the molecular components of the NF-κB pathway that are affected by this kinase. Our results revealed that CLK3 mitigated the phosphorylation/activation of transforming growth factor-α-activated kinase 1 (TAK1), inhibitor of NF-κB kinase alpha/beta (IKKα/α), NF-κB p65 (RelA), NF-κB inhibitor alpha (IκBα), and Extracellular signal-regulated kinase 1/2-Mitogen-activated protein kinase (ERK1/2-MAPK), suggesting that CLK3 inhibits both the NF-κB and MAPK signaling activated by TNFα exposure. Further studies are required to elucidate the mechanism by which CLK3 inhibits the canonical and non-canonical NF-κB pathways. Collectively, these findings reveal CLK3 as a novel negative regulator of NF-κB signaling.

• Journal of the Korean earth science society
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• v.39 no.6
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• pp.519-532
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• 2018

We investigated the effect of galactic plane toward molecular motion and kinematics in the northern filament (NF) of Orion Molecular Clouds Complex (OMC) using $^{12}CO$ (J=1-0) line. Observed data were from three areas including NF1, NF2, and NF3 in far-out order from galactic plane, for a total 270 hours by Seoul National University Radio Astronomy Observatory (SRAO) 6m telescope, with 2arcmin spatial resolution. galactic plane and OMC NF were connected to each other along the magnetic field at a density of 3% for $^{12}CO$ (J=2-1) and 9% for the case of dust. $^{12}CO$ (J=1-0), $^{12}CO$ (J=2-1), and interstellar dusts were distributed uniformly in NF3, but only in certain regions with relatively high density in NF1 and NF2. NF showed a single structure, partial shrinking motion in NF1, and rotational motion at the bottom of NF2, and spiral rotation associated with magnetic field only in NF3. The position-velocity analysis showed that the materials including $^{12}CO$ (J=1-0) could flow toward galactic plane along NF2 and NF3. However, there was no clear cause for the material to flow toward galactic plane in this result. Further detailed observation for rotational motion at the top of NF1 and NF2 might help to confirm it.

• Molecules and Cells
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• v.37 no.3
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• pp.189-195
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• 2014

The NF-${\kappa}B$ pathway transcriptionally controls a large set of target genes that play important roles in cell survival, inflammation, and immune responses. While many studies showed anti-tumorigenic and pro-survival role of NF-${\kappa}B$ in cancer cells, recent findings postulate that NF-${\kappa}B$ participates in a senescence-associated cytokine response, thereby suggesting a tumor restraining role of NF-${\kappa}B$. In this review, we discuss implications of the NF-${\kappa}B$ signaling pathway in cancer. Particularly, we emphasize the connection of NF-${\kappa}B$ with cellular senescence as a response to chemotherapy, and furthermore, present examples how distinct oncogenic network contexts surrounding NF-${\kappa}B$ produce fundamentally different treatment outcomes in aggressive B-cell lymphomas as an example.

• BMB Reports
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• v.44 no.8
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• pp.553-557
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• 2011

We previously reported that CDK2/Cyclin A can phosphorylate and activate the transcription factor NF-Y. In this study, we investigated a potential regulatory role for NF-Y in the transcription of Cyclin A and other cell cycle regulatory genes. Gel-shift assays demonstrate that NF-Y binds to CCAAT sequences in the Cyclin A promoter, as well as to those in the promoters of cell cycle G2 regulators such as CDC2, Cyclin B and CDC25C. Furthermore, expression of Cyclin A increases NF-Y's affinity for CCAAT sequences in the CDC2 promoter; however, Cyclin A's induction of CDC2 transcription is antagonized by p21, an inhibitor of CDK2/Cyclin A. These results suggest a model wherein NF-Y binds to and activates transcription from the Cyclin A promoter, increasing cellular levels of Cyclin A/CDK2 and potentiating NF-Y's capacity for transcriptional transactivation, and imply a positive feedback loop between NF-Y and Cyclin A/CDK2. Our findings are additionally indicative of a role for Cyclin A in activating Cyclin B/CDK1 through promoting NF-Y dependent transcription of Cyclin B and CDC2; NF-Y mediated crosstalk may therefore help to orchestrate cell-cycle progression.

• Biomedical Science Letters
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• v.12 no.4
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• pp.413-418
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• 2006

Charcot-Marie-Tooth disease (CMT) is blown as one of the inherited disorder of peripheral nervous system. Recently, it was found that point mutations in the neurofilament light subunit (NF-L) gene cause CMT. Neurofilaments (NFs) are heteropolymers consist of NF-L, NF-M and NF-H. To assess the relationship between CMT and NF-L mutation in cellular level, we performed phenotypic analysis of the mutant NF-L (E397K) using cultured cell lines. Vimentin-deficient human adrenal carcinoma SW13 (Vim-) cells have a potential to form the intermediate filaments when the cells are expressing both NF-L and NF-M. Our results show that co-expression of wild type NF-L with NF-M showed intermediate filament formation in SW13 (Vim-) cells, while E397K with NF-M did not. This result means that E397K mutant lost its ability to form the intermediate filament in vivo, and further suggests that the E397K mutation is closely related to CMT.