• Distinctive contribution of two additional residues in protein aggregation of Aβ42 and Aβ40 isoforms

    Amyloid-β (Aβ) aggregation. (A) The primary structure of Aβ42 and aggregation mechanism of Aβ. Unstructured monomeric Aβ proteins self-assemble to oligomeric states; the oligomeric intermediates then elongate to insoluble fibrils. (B) Trajectories of Aβ biomarker abnormality and AD progression. Aβ as a biomarker can be assessed using cerebrospinal fluid Aβ and PET Aβ imaging. Aβ the panel image was adopted and reformatted from the review by Sperling et al. (26). (C) Enzymatic hydrolysis of amyloid-β precursor protein (APP) following non-pathogenic/pathogenic cleavage pathway. APP is sequentially cleaved by β-secretase and γ-secretase. As a result of the sequential cleavage, Aβ 1-42 (Aβ42) or Aβ 1-40 (Aβ40) is released to the extracellular space of neuronal cells. The inset of panel c shows the cleavage pathways of Aβ42/Aβ40 by γ-secretase.
  • Emerging paradigms in cancer cell plasticity

    The significance of EMT in cancer metastasis. (A) A schematic overview illustrating the mechanistic details of epithelial-to-mesenchymal transition (EMT). During EMT, cell transition from an epithelial state to a mesenchymal state, marked by the loss of cell-to-cell adhesions and the acquisition of migratory characteristics. The verification of EMT often involves examining substantial changes in the expression of epithelial markers like E-cadherin, Occludins, and Cytokeratin, as well as mesenchymal markers such as N-cadherin and vimentin. (B) The significant functions of EMT on the invasive progression of cancer metastasis. EMT triggers the activation of protein hydrolases, including matrix metalloproteinases (MMPs), to amplify the migratory capabilities of tumor cells. Additionally, the EMT mechanism expedites the liberation of circulating tumor cells (CTCs) by fostering angiogenesis.

BMB Reports 2024; 57(6): 263~310
Invited Mini Reviews
Distinctive contribution of two additional residues in protein aggregation of Aβ42 and Aβ40 isoforms
Dongjoon Im & Tae Su Choi
BMB Reports 2024; 57(6): 263-272  https://doi.org/10.5483/BMBRep.2024-0044
Emerging paradigms in cancer cell plasticity
Hyunbin D. Huh & Hyun Woo Park
BMB Reports 2024; 57(6): 273-280  https://doi.org/10.5483/BMBRep.2024-0018
Integrative analysis of microRNA-mediated mitochondrial dysfunction in hippocampal neural progenitor cell death in relation with Alzheimer’s disease
A Reum Han, Tae Kwon Moon, Im Kyeung Kang, Dae Bong Yu , Yechan Kim, Cheolhwan Byon, Sujeong Park , Hae Lin Kim, Kyoung Jin Lee, Heuiran Lee , Ha-Na Woo & Seong Who Kim
BMB Reports 2024; 57(6): 281-286  https://doi.org/10.5483/BMBRep.2023-0167
CDKN2 expression is a potential biomarker for T cell exhaustion in hepatocellular carcinoma
Shibo Wei , Yan Zhang , Baeki E. Kang , Wonyoung Park , He Guo , Seungyoon Nam , Jong-Sun Kang , Jee-Heon Jeong , Yunju Jo , Dongryeol Ryu , Yikun Jiang & Ki-Tae Ha
BMB Reports 2024; 57(6): 287-292  https://doi.org/10.5483/BMBRep.2023-0214
Genetic disruption of ATAT1 causes RhoA downregulation through abnormal truncation of C/EBPβ
Jee-Hye Choi, Jangho Jeong, Jaegu Kim, Eunae You, Seula Keum, Seongeun Song, Ye Eun Hwang, Minjoo Ji, Kwon-Sik Park & Sangmyung Rhee
BMB Reports 2024; 57(6): 293-298  https://doi.org/10.5483/BMBRep.2023-0230
Tumor antigen PRAME is a potential therapeutic target of p53 activation in melanoma cells
Yong-Kyu Lee, Hyeon Ho Heo, Nackhyoung Kim, Ui-Hyun Park, Hyesook Youn, Eun-Yi Moon, Eun-Joo Kim & Soo-Jong Um
BMB Reports 2024; 57(6): 299-304  https://doi.org/10.5483/BMBRep.2023-0246
T-plastin contributes to epithelial-mesenchymal transition in human lung cancer cells through FAK/AKT/Slug axis signaling pathway
Soon Yong Park , Hyeongrok Choi , Soo Min Choi, Seungwon Wang, Sangin Shim, Woojin Jun, Jungkwan Lee  & Jin Woong Chung
BMB Reports 2024; 57(6): 305-310  https://doi.org/10.5483/BMBRep.2024-0040


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June 2024
Volume 57
Issue 6

2023 SCI Impact Factor 2.9


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