• Highlighted STAT3 as a potential drug target for cancer therapy

    STAT3 signaling in cancer. STAT3 signaling is activated by binding of various ligands to their cell surface receptors, leading to phosphorylation of STAT3. STAT3 also directly phosphorylated by Src and Abl, which are non-receptor tyrosine kinases. Phosphorylated STAT3 further homo-dimerized and translocated, to the nucleus. STAT3 regulate CyclinD1, c-Myc, Survivin, Bcl-XL, and Mcl1, which regulate cellular proliferation and survival. STAT3 up-regulates VEGF, bFGF, HGF, and HIF1α. Additionally, STAT3 also regulates MMP2, MMP9, Twist, and Vimentin, for invasion and migration. STAT3 activation also downregulates immune surveillance, by secretion of pro-inflammatory cytokines. Furthermore, maintaining cancer stem cell properties, STAT3 regulates Oct3/4, Nanog, CD133, and CD44.
  • mTOR signalling pathway - A root cause for idiopathic autism?

    Schematic representation of various molecular inhibitors and stimulators in mTOR signalling pathway. PTEN and NF1 could inhibit the activation of AKT. AKT when mutated could inhibit the activation of TSC 1 and TSC 2 that are precursors of mTORC1. FMRP inhibition could lead to deactivation of mTORC2. When stimulated, mTORC1 is involved in various cellular processes including microtubule organisation, autophagy, lipid biosynthesis, RNA biosynthesis, and protein synthesis using precursors of CLIP-170, ULK1, Lipin-1, TFEB, and P70S6K, respectively. Stimulation of mTORC2 leads to proper cytoskeletal organisation through RAC, Rho, and PKC. Cell survival is achieved through SGK1.

BMB Reports 2019; 52(7): 415~474
Invited Mini Reviews
Highlighted STAT3 as a potential drug target for cancer therapy
Haeri Lee, Ae Jin Jeong & Sang-Kyu Ye
BMB Reports 2019; 52(7): 415-423  https://doi.org/10.5483/BMBRep.2019.52.7.152
mTOR signalling pathway - A root cause for idiopathic autism?
Harsha Ganesan, Venkatesh Balasubramanian, Mahalaxmi Iyer, Anila Venugopal, Mohana Devi Subramaniam, Ssang-Goo Cho & Balachandar Vellingiri
BMB Reports 2019; 52(7): 424-433  https://doi.org/10.5483/BMBRep.2019.52.7.137
2-(trimethylammonium)ethyl (R)-3-methoxy-3-oxo-2-stearamidopropyl phosphate enhances thrombopoietin–induced megakaryocytic differentiation and plateletogenesis
Jusong Kim, Guanghai Jin, Jisu Lee, Kyeong Lee, Yun Soo Bae & Jaesang Kim
BMB Reports 2019; 52(7): 434-438  https://doi.org/10.5483/BMBRep.2019.52.7.200
Protective effects of N,4,5-trimethylthiazol-2-amine hydrochloride on hypoxia-induced β-amyloid production in SH-SY5Y cells
A Reum Han, Ji Woong Yang, Jung-Min Na, Soo Young Choi & Sung-Woo Cho
BMB Reports 2019; 52(7): 439-444  https://doi.org/10.5483/BMBRep.2019.52.7.231
Surface expression of TTYH2 is attenuated by direct interaction with β-COP
Jiwon Ryu, Dong-Gyu Kim, Young-Sun Lee, Yeonju Bae, Ajung Kim, Nammi Park, Eun Mi Hwang & Jae-Yong Park
BMB Reports 2019; 52(7): 445-450  https://doi.org/10.5483/BMBRep.2019.52.7.188
High NDRG3 expression facilitates HCC metastasis by promoting nuclear translocation of β-catenin
JiKui Shi, HongZhen Zheng & LingYan Yuan
BMB Reports 2019; 52(7): 451-456  https://doi.org/10.5483/BMBRep.2019.52.7.201
ATAD2 expression increases [18F]Fluorodeoxyglucose uptake value in lung adenocarcinoma via AKT-GLUT1/HK2 pathway
Tong Sun, Bulin Du, Yao Diao, Xuena Li, Song Chen & Yaming Li*
BMB Reports 2019; 52(7): 457-462  https://doi.org/10.5483/BMBRep.2019.52.7.042
Expression and secretion of CXCL12 are enhanced in autosomal dominant polycystic kidney disease
Hyunho Kim, Jinmo Sung, Hyunsuk Kim, Hyunjin Ryu, Hayne Cho Park, Yun Kyu Oh, Hyun-Seob Lee, Kook-Hwan Oh & Curie Ahn
BMB Reports 2019; 52(7): 463-468  https://doi.org/10.5483/BMBRep.2019.52.7.112
The IRF2BP2-KLF2 axis regulates osteoclast and osteoblast differentiation
Inyoung Kim, Jung Ha Kim, Kabsun Kim, Semun Seong & Nacksung Kim
BMB Reports 2019; 52(7): 469-474  https://doi.org/10.5483/BMBRep.2019.52.7.104


Current Issue

July 2019
Volume 52
Issue 7

2018 SCI Impact Factor 2.966


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