Bora Kim

Publications (2)11.18 Total impact

• Source

  Available from: Young Kee Shin

  Article: Cancer-associated splicing variant of tumor suppressor AIMP2/p38: pathological implication in tumorigenesis.

  Jin Woo Choi, Dae Gyu Kim, Al-Eum Lee, Hye Rim Kim, Jin Young Lee, Nam Hoon Kwon, Young Kee Shin, Soon-Kyung Hwang, Seung-Hee Chang, Myung-Haing Cho, [......], Jhingook Kim, Seung Hyun Oh, Bora Kim, Soo-Youl Kim, Hyo-Sung Jeon, Jae Yong Park, Hyunseok Peter Kang, Bum Joon Park, Jung Min Han, Sunghoon Kim
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  ABSTRACT: Although ARS-interacting multifunctional protein 2 (AIMP2, also named as MSC p38) was first found as a component for a macromolecular tRNA synthetase complex, it was recently discovered to dissociate from the complex and work as a potent tumor suppressor. Upon DNA damage, AIMP2 promotes apoptosis through the protective interaction with p53. However, it was not demonstrated whether AIMP2 was indeed pathologically linked to human cancer. In this work, we found that a splicing variant of AIMP2 lacking exon 2 (AIMP2-DX2) is highly expressed by alternative splicing in human lung cancer cells and patient's tissues. AIMP2-DX2 compromised pro-apoptotic activity of normal AIMP2 through the competitive binding to p53. The cells with higher level of AIMP2-DX2 showed higher propensity to form anchorage-independent colonies and increased resistance to cell death. Mice constitutively expressing this variant showed increased susceptibility to carcinogen-induced lung tumorigenesis. The expression ratio of AIMP2-DX2 to normal AIMP2 was increased according to lung cancer stage and showed a positive correlation with the survival of patients. Thus, this work identified an oncogenic splicing variant of a tumor suppressor, AIMP2/p38, and suggests its potential for anti-cancer target.
  PLoS Genetics 03/2011; 7(3):e1001351. · 8.69 Impact Factor
• Article: Transglutaminase 2 gene ablation protects against renal ischemic injury by blocking constant NF-κB activation.

  Dae-Seok Kim, Bora Kim, Hongmin Tahk, Dong-Hyun Kim, Eu-Ree Ahn, Changsun Choi, Yoon Jeon, Seo Young Park, Ho Lee, Seung Hyun Oh, Soo-Youl Kim
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  ABSTRACT: Transglutaminase 2 knockout (TGase2(-/-)) mice show significantly reduced inflammation with decreased myofibroblasts in a unilateral ureteral obstruction (UUO) model, but the mechanism remains to be clarified. Nuclear factor-κB (NF-κB) activation plays a major role in the progression of inflammation in an obstructive nephropathy model. However, the key factors extending the duration of NF-κB activation in UUO are not known. In several inflammatory diseases, we and others recently found that TGase 2 plays a key role in extending NF-κB activation, which contributes to the pathogenesis of disease. In the current study, we found that NF-κB activity in mouse embryogenic fibroblasts (MEFs) from TGase2(-/-) mice remained at the control level while the NF-κB activity of wild-type (WT) MEFs was highly increased under hypoxic stress. Using the obstructive nephropathy model, we found that NF-κB activity remained at the control level in TGase2(-/-) mouse kidney tissues, as measured by COX-2 expression, but was highly increased in WT tissues. We conclude that TGase 2 gene ablation reduces the duration of NF-κB activation in ischemic injury.
  Biochemical and Biophysical Research Communications 12/2010; 403(3-4):479-84. · 2.48 Impact Factor