Evaluation of Phoxilium® to Prevent HypoPHOSPHATEmia compared to Hemosol B0® or Prismocol B22 during Citrate-based Continuous Renal Replacement Therapy (CRRT) in the Intensive Care Unit (ICU)

开始日期2023-12-05

申办/合作机构

Austin Health

100 项与 NF-κB x MAP3K14 相关的临床结果

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100 项与 NF-κB x MAP3K14 相关的转化医学

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0 项与 NF-κB x MAP3K14 相关的专利（医药）

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项与 NF-κB x MAP3K14 相关的文献（医药）

2023-09-01·Genomics

EGR1 knockdown confers protection against ferroptosis and ameliorates intervertebral disc cartilage degeneration by inactivating the MAP3K14/NF-κB axis.

Article

作者: Gao, Jian ; He, Liming ; Zhang, Erlei ; Zhang, Jianguo ; Feng, Haoyu ; Li, Qiang

This study explored whether EGR1-MAP3K14-NF-κB axis regulated ferroptosis and IVD cartilage generation. EGR1 and MAP3K14 expression levels were determined in CEP tissues of IVDD patients and intermittent cyclic mechanical tension (ICMT)-treated CEP cells. After EGR1 and MAP3K14 were altered in ICMT-treated CEP cells, the expression levels of degeneration- and ferroptosis-related proteins were measured. Binding relationship between EGR1 and MAP3K14 was evaluated. Additionally, the impacts of EFR1 knockdown on ferroptosis and cartilage degeneration in vivo were analyzed. EGR1 and MAP3K14 were overexpressed in clinical samples and cell models of IVDD. In IVDD cell models, EGR1 knockdown reduced ferroptosis and cartilage degeneration, which was reversed by MAP3K14 overexpression or Erastin treatment. NF-κB pathway inhibition nullified these effects of sh-EGR1 + oe-MAP3K14 treatment. EGR1 knockdown inhibited ferroptosis and relieved CEP degeneration via MAP3K14-NF-κB axis inactivation in vivo. Collectively, our findings highlighted that EGR1 promoted ferroptosis and IVD cartilage degeneration through MAP3K14-NF-κB axis.

2023-03-07·Research square

Transcriptional Induction of NF-kB-Inducing Kinase by E2F4/5 Facilitates Collective Invasion of Glioma Cells.

作者: McFadden, Kassandra ; Pflug, Kathryn ; Sitcheran, Raquel ; Herrera, Linda ; Lee, Dong

The prognosis of high-grade gliomas, such as glioblastoma multiforme (GBM), is extremely poor due to the highly invasive nature of these aggressive cancers. Previous work has demonstrated that TNF-weak like factor (TWEAK) induction of the noncanonical NF-κB pathway increases the invasiveness of glioma cells in an NF-κB-inducing kinase (NIK)-dependent manner. While NIK activity is predominantly regulated at the posttranslational level, we show here that NIK ( MAP3K14 ) is upregulated at the transcriptional level in invading cell populations, with the highest expression observed in the most invasive cells. Glioma cells with high induction of NIK gene expression demonstrate characteristics of collective invasion, facilitating invasion of neighboring cells. Furthermore, we demonstrate that the E2F transcription factors E2F4 and E2F5 directly regulate NIK transcription and are required to promote glioma cell invasion in response to TWEAK. Overall, our findings demonstrate that transcriptional induction of NIK facilitates collective cell migration and invasion, thereby promoting glioma pathogenesis.

2023-01-01·Frontiers in immunology

Inhibition of non-canonical NF-κB signaling suppresses periodontal inflammation and bone loss

Article

作者: Nishimura, Fusanori ; Takakura-Hino, Nana ; Li, Aonan ; Yang, Nan ; Mukai, Satoru ; Matsuda, Miho ; Aoki, Tsukasa ; Jimi, Eijiro ; Hiura, Fumitaka

Periodontal disease is an infectious disease that affects many people worldwide.Disease progression destroys the alveolar bone and causes tooth loss.We have previously shown that alymphoplasia (aly/aly) mice harboring a loss-of-function mutation in the map3k14 gene, which is involved in p100 to p52 processing of the alternative NF-κB pathway, exhibited mild osteopetrosis due to decreased number of osteoclasts, suggesting the alternative NF-κB pathway as a potential drug target for the amelioration of bone disease.In the present study, wild-type (WT) and aly/aly mice were subjected to silk ligation to establish a periodontitis model.Alveolar bone resorption was suppressed in aly/aly mice by decreased numbers of osteoclasts in the alveolar bone in comparison to WT mice.Furthermore, the expression of receptor activator of NF-κB ligand (RANKL) and TNFα (cytokines involved in osteoclast induction in periligative gingival tissue) was decreased.When primary osteoblasts (POBs) and bone marrow cells (BMCs) derived from WT and aly/aly mice were prepared and co-cultured, osteoclasts were induced from WT-derived BMCs, regardless of the origin of the POBs, but hardly formed from aly/aly mouse-derived BMCs.Furthermore, the local administration of an NIK inhibitor, Cpd33, inhibited osteoclast formation and thereby inhibited alveolar bone resorption in the periodontitis model.Therefore, the NIK-mediated NF-κB alternative pathway can be a therapeutic target for periodontal disease.