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From Wikipedia, the free encyclopedia
In this Korean name, the family name is Kaang.
Bong-Kiun Kaang
Born1961 (age 62–63)
Jeju-do, South Korea
Nationality South Korean
Alma materB.S. Seoul National University (1984)

M.S. Seoul National University (1986) Ph.D. Columbia University (1992)

Postdoctoral Research Fellow, Center for Neurobiology and Behavior, Columbia University (1992 - 1994)
Known for Aplysia, Neuroscience, Learning and Memory
AwardsBest Research Award, College of Natural Sciences, Seoul National University (2007)
Excellent Research Scientist, Korea Ministry of Science and Technology (2007)
Life Science Award, Korean Society for Molecular and Cellular Biology (2008)
Fellow of the Korean Academy of Science and Technology (2010)
Scientific career
Fields Neuroscience
Institutions Seoul National University, Dept. of Biological Sciences & Brain and Cognitive Sciences
Doctoral advisor Eric R. Kandel, M.D.(Nobel Laureate, 2000)
Kaang Bong-kiun
Hangul
강봉균
Hanja
Revised RomanizationGang Bong-gyun
McCune–ReischauerKang Ponggyun

Kaang Bong-Kiun (born November 21, 1961) is a South Korean professor of neuroscience in the Department of Biological Sciences of Seoul National University. He is a fellow of the Korean Academy of Science and Technology and co-director of the IBS Center for Cognition and Sociality with Changjoon Justin Lee.

Early life and education

Kaang was born in Jeju-do, South Korea, on November 21, 1961. He received his bachelor's degree in 1984 and his M.S. in 1986 from the Department of Microbiology, Seoul National University. During his M.S. course, he developed an interest in molecular neuroscience, particularly, in how memory is stored in the brain at the molecular level. He then went to Columbia University where he was supervised by a Nobel laureate Eric R. Kandel for his Ph.D. course and a brief postdoctoral study. He investigated the molecular mechanisms of learning and memory using a simple animal, the marine snail Aplysia. Under the supervision of Dr. Kandel, he received his Ph.D. in 1992. Kaang's Ph.D. thesis, which was entitled, “Studies of Long-Term Facilitation Using Gene Transfer Methods,” introduced the development of the gene delivery system in Aplysia neurons. He continued his research as a postdoctoral research fellow at the Center for Neurobiology and Behavior at Columbia University until 1994, when he was appointed to a faculty position at Seoul National University, Korea.

Work

Kaang's studies have mainly focused on the molecular mechanisms of learning and memory. In his Ph.D. course, he developed the microinjection-based gene transfer method for Aplysia neurons. This technology opened up a new era of molecular studies on the memory mechanisms in Aplysia, as well as of functional studies of receptors, signaling molecules, and ion channels, which play key roles in neuronal functions. He revealed that serotonin-induced transcription requires the protein kinase-A-mediated phosphorylation of the cAMP-response element-binding protein (CREB). Moreover, he found that multiple pulses of serotonin stimulate gene expression that is mediated by the cAMP-response element (CRE). [1] [2]

He continued to study Aplysia when he set up his own laboratory in Korea. He started by establishing an expressed sequence tag database and transcriptome analyses of Aplysia. He identified a serotonin receptor involved in learning-related synaptic facilitation in Aplysia. In addition, he was successful in finding the novel signaling molecules ApLLP, CAMAP, ApPDE4, and ApAUF1, which are involved in long-term facilitation. With his colleagues at Columbia University, he delineated the molecular networks of the molecules that interplay with other regulatory molecules, such as ApCAM, CREB1, CREB2, C/EBP, and ApAF. Furthermore, Kaang reported that, by genetically controlling the expression of these key molecules in specific neurons, he could induce long-term facilitation that lasted days with a single pulse of serotonin that normally induces short-term facilitation that lasts only several minutes. [3] [4] [5] [6] [7] [8] [9] [10] [11]

In parallel with these studies in Aplysia, Kaang has expanded his research field to more complex mammalian models. Combining molecular, electrophysiological, and behavioral experimental tools, he began to explore the mechanisms of learning and memory in mice. One of the major findings from his group was proving the importance of synaptic protein degradation in memory reorganization. He found that postsynaptic proteins were degraded in the hippocampus by polyubiquitination after the retrieval of contextual fear memory. Moreover, the infusion of proteasome inhibitors into the CA1 of the hippocampus immediately after retrieval prevented anisomycin-induced memory impairment and the extinction of fear memory. Another major finding from his laboratory was the importance of a kinase, PI3Kγ, in long-term depression and behavioral flexibility. [12] [13] [14]

His interests also include neurological symptoms such as pain and itch and psychiatric disorders, such as autism. One of his major investigations regarding pain was proving that PKMζ, a molecule known for its role in the maintenance of long-term potentiation and long-term memory, is important in maintaining chronic pain in the anterior cingulate cortex. In collaboration with Min Zhuo from the University of Toronto, he showed that the phosphorylation of PKMζ was increased in a neuropathic pain model in the anterior cingulate cortex. In addition, they showed that chronic pain behavior was alleviated by treating mice with the PKMζ blocker ZIP, suggesting that this could be a new therapeutic target for treating chronic pain. [15] [16] [17] [18]

In collaboration with M.G. Lee and E. Kim, he demonstrated that NMDAR-dependent synaptic plasticity in the hippocampus is impaired in a mouse model of autism, the Shank2 knockout. When they treated the mice with drugs that upregulate NMDA receptor function, the impairment was recovered, suggesting the possibility that these drugs could be used for treating patients with autism in the future. [19]

Kaang has published 110 research and review articles in a number of journals, including Nature, Science, Cell, Neuron, and Nature Neuroscience. He has been the editor-in-chief of Molecular Brain. Kaang received the Life Science Award from the Korean Society for Molecular and Cellular Biology in 2008. He was awarded the Donghun Award from the Korean Society for Biochemistry and Molecular Biology in 2012. He also won the Kyung-Ahm Prize in the same year from the Kyung Ahm Foundation.

Awards

References

  1. ^ Kaang BK, Pfaffinger PI, Grant SG, Kandel ER, Furukawa Y (1992). "Overexpression of an Aplysia shaker K+channel gene modifies the electrical properties and synaptic efficacy of identified Aplysia neurons". Proc Natl Acad Sci USA. 89 (3): 1133–1137. Bibcode: 1992PNAS...89.1133K. doi: 10.1073/pnas.89.3.1133. PMC  48400. PMID  1310540.
  2. ^ Kaang BK, Kandel ER, Grant SG (1993). "Activation of cAMP-responsive genes by stimuli that produce long-term facilitation in Aplysia sensory neurons". Neuron. 10 (3): 427–435. doi: 10.1016/0896-6273(93)90331-k. PMID  8384857. S2CID  5520552.
  3. ^ Lee YS, Choi SL, Lee SH, Kim H, Park H, Lee N, Lee SH, Chae YS, Jang DJ, Kandel ER, Kaang BK (2009). "Identification of a serotonin receptor coupled to adenylyl cyclase involved in learning related heterosynaptic facilitation in Aplysia". Proc Natl Acad Sci USA. 106 (34): 14634–14639. Bibcode: 2009PNAS..10614634L. doi: 10.1073/pnas.0907502106. PMC  2732834. PMID  19706550.
  4. ^ Kim H, Lee SH, Han JH, Lee JA, Cheang YH, Chang DJ, Lee YS, Kaang BK (2006). "A nucleolar protein ApLLP induces ApC/EBP expression required for long-term synaptic facilitation in Aplysia neurons". Neuron. 49 (5): 707–718. doi: 10.1016/j.neuron.2006.01.035. PMID  16504946.
  5. ^ Lee SH, Lim CS, Park H, Lee JA, Han JH, Kim H, Cheang YH, Lee SH, Lee YS, Ko HG, Jang DH, Kim H, Miniaci MC, Bartsch D, Kim E, Bailey CH, Kandel ER, Kaang BK (2007). "Nuclear translocation of CAM-associated protein activates transcription for long-term facilitation in Aplysia". Cell. 129 (4): 801–812. doi: 10.1016/j.cell.2007.03.041. PMID  17512412.
  6. ^ Lee YS, Choi SL, Jun H, Yim SJ, Lee JA, Kim HF, Lee SH, Shim J, Lee K, Jang DJ, Kaang BK (2012). "AU-rich element-binding protein negatively regulates CCAAT enhancer-binding protein mRNA stability during long-term synaptic plasticity in Aplysia". Proc Natl Acad Sci USA. 109 (38): 15520–15525. Bibcode: 2012PNAS..10915520L. doi: 10.1073/pnas.1116224109. PMC  3458389. PMID  22949683.
  7. ^ Jang DJ, Park SW, Lee JA, Lee C, Chae YS, Park H, Kim MJ, Choi SL, Lee N, Kim H, Kaang BK (2010). "N termini of apPDE4 isoforms are responsible for targeting the isoforms to different cellular membranes". Learn Mem. 17 (9): 469–479. doi: 10.1101/lm.1899410. PMID  20813835.
  8. ^ Lee JA, Kim H, Lee YS, Kaang BK (2003). "Overexpression and RNA interference of Ap-cyclic AMP-response element binding protein-2, a repressor of long-term facilitation, in Aplysia kurodai sensory-to-motor synapses". Neurosci Lett. 337 (1): 9–12. doi: 10.1016/s0304-3940(02)01285-5. PMID  12524159. S2CID  17255313.
  9. ^ Lee JA, Kim HK, Kim KH, Han JH, Lee YS, Lim CS, Chang DJ, Kubo T, Kaang BK (2001). "Overexpression of and RNA interference with the CCAAT enhancer-binding protein on long-term facilitation of Aplysia sensory to motor synapses". Learn Mem. 8 (4): 220–226. doi: 10.1101/lm.40201. PMC  311377. PMID  11533225.
  10. ^ Lee JA, Lee SH, Lee CH, Chang DJ, Lee Y, Kim H, Cheang YH, Ko HG, Lee YS, Jun HJ, Bartsch D, Kandel ER, Kaang BK (2006). "PKA-activated ApAF-ApC/EBP heterodimer is a key downstream effector of ApCREB and is necessary and sufficient for the consolidation of long-term facilitation". J Cell Biol. 174 (6): 827–838. doi: 10.1083/jcb.200512066. PMC  2064337. PMID  16966424.
  11. ^ Lee YS, Bailey CH, Kandel ER, Kaang BK (2008). "Transcriptional regulation of long-term memory in the marine snail Aplysia". Mol Brain. 1: 3. doi: 10.1186/1756-6606-1-3. PMC  2546398. PMID  18803855.
  12. ^ Lee SH, Choi JH, Lee N, Lee HR, Kim JI, Yu NK, Choi SL, Lee SH, Kim H, Kaang BK (2008). "Synaptic Protein Degradation Underlies Destabilization of Retrieved Fear Memory". Science. 319 (5867): 1253–1259. Bibcode: 2008Sci...319.1253L. doi: 10.1126/science.1150541. PMID  18258863. S2CID  45611862.
  13. ^ Kaang BK, Lee SH, Kim H (2009). "Synaptic Protein Degradation as a Mechanism in Memory Reorganization". Neuroscientist. 15 (5): 430–435. doi: 10.1177/1073858408331374. PMID  19264729. S2CID  18724901.
  14. ^ Kim JI, Lee HR, Sim SE, Baek J, Yu NK, Choi JH, Ko HG, Lee YS, Park SW, Kwak C, Ahn SJ, Choi SY, Kim H, Kim KH, Backx PH, Bradley CA, Kim E, Jang DJ, Lee K, Kim SJ, Zhuo M, Collingridge GL, Kaang BK (2011). "PI3K is required for NMDAR-dependent long-term depression and behavioral flexibility". Nat Neurosci. 14 (11): 1447–1454. doi: 10.1038/nn.2937. PMID  22019731. S2CID  16198101.
  15. ^ Li XY; Ko HG; Chen T; Descalzi G; Koga K; Wang H; Kim SS; Shang Y; Kwak C; Park SW; Shim J; Lee K; Collingridge GL; Kaang BK*; Zhuo M.* (2010). "Alleviating neuropathic pain hypersensitivity by inhibiting PKMζ in the anterior cingulate cortex". Science. 330 (6009): 1400–1404. Bibcode: 2010Sci...330.1400L. doi: 10.1126/science.1191792. PMID  21127255. S2CID  5125595.
  16. ^ Lee B, Baek BJ, Deslcazi G, Kim JI, Lee HR, Lee K, Kaang BK, Zhuo M (2011). "Enhanced itch responses in mice lacking phosphoinositide 3-kinase-γ". Mol Pain. 7: 1744–8069–7–96. doi: 10.1186/1744-8069-7-96. PMC  3261823. PMID  22168443.
  17. ^ Kang SJ; Liu MG; Chen T; Ko HG; Baek GC; Lee HR; Lee K; Collingridge GL; Kaang BK*; Min Zhuo*. (2012). "Plasticity of metabotropic glutamate receptor dependent long-term depression in the ACC after amputation". J Neurosci. 32 (33): 11318–11329. doi: 10.1523/jneurosci.0146-12.2012. PMC  6621183. PMID  22895715.
  18. ^ Lee B, Baek BJ, Deslcazi G, Kim JI, Lee HR, Lee K, Kaang BK, Zhuo M (2011). "Enhanced itch responses in mice lacking phosphoinositide 3-kinase-γ" (PDF). Mol Pain. 7: 1744–8069–7–96. doi: 10.1186/1744-8069-7-96. PMC  3261823. PMID  22168443.
  19. ^ Won H; Lee HR; Gee HY; Mah W; Kim JI; Lee J; Ha S; Chung C; Jung ES; Cho YS; Park SG; Lee JS; Lee K; Kim D; Bae YC; Kaang BK*; Lee MG*; Kim E*. (June 2012). "Autistic-like social behaviour in Shank2-mutant mice improved by restoring NMDA receptor function". Nature. 486 (7402): 261–265. Bibcode: 2012Natur.486..261W. doi: 10.1038/nature11208. PMID  22699620. S2CID  4423977.
  20. ^ 원호섭 (25 June 2018). "최고과학기술인상에 강봉균·박진수". 매일경제 (in Korean). Retrieved 16 November 2023.

Publications

External links

Retrieved from " https://en.wikipedia.org/?title=Kaang_Bong-kiun&oldid=1223929645"
From Wikipedia, the free encyclopedia
In this Korean name, the family name is Kaang.
Bong-Kiun Kaang
Born1961 (age 62–63)
Jeju-do, South Korea
Nationality South Korean
Alma materB.S. Seoul National University (1984)

M.S. Seoul National University (1986) Ph.D. Columbia University (1992)

Postdoctoral Research Fellow, Center for Neurobiology and Behavior, Columbia University (1992 - 1994)
Known for Aplysia, Neuroscience, Learning and Memory
AwardsBest Research Award, College of Natural Sciences, Seoul National University (2007)
Excellent Research Scientist, Korea Ministry of Science and Technology (2007)
Life Science Award, Korean Society for Molecular and Cellular Biology (2008)
Fellow of the Korean Academy of Science and Technology (2010)
Scientific career
Fields Neuroscience
Institutions Seoul National University, Dept. of Biological Sciences & Brain and Cognitive Sciences
Doctoral advisor Eric R. Kandel, M.D.(Nobel Laureate, 2000)
Kaang Bong-kiun
Hangul
강봉균
Hanja
Revised RomanizationGang Bong-gyun
McCune–ReischauerKang Ponggyun

Kaang Bong-Kiun (born November 21, 1961) is a South Korean professor of neuroscience in the Department of Biological Sciences of Seoul National University. He is a fellow of the Korean Academy of Science and Technology and co-director of the IBS Center for Cognition and Sociality with Changjoon Justin Lee.

Early life and education

Kaang was born in Jeju-do, South Korea, on November 21, 1961. He received his bachelor's degree in 1984 and his M.S. in 1986 from the Department of Microbiology, Seoul National University. During his M.S. course, he developed an interest in molecular neuroscience, particularly, in how memory is stored in the brain at the molecular level. He then went to Columbia University where he was supervised by a Nobel laureate Eric R. Kandel for his Ph.D. course and a brief postdoctoral study. He investigated the molecular mechanisms of learning and memory using a simple animal, the marine snail Aplysia. Under the supervision of Dr. Kandel, he received his Ph.D. in 1992. Kaang's Ph.D. thesis, which was entitled, “Studies of Long-Term Facilitation Using Gene Transfer Methods,” introduced the development of the gene delivery system in Aplysia neurons. He continued his research as a postdoctoral research fellow at the Center for Neurobiology and Behavior at Columbia University until 1994, when he was appointed to a faculty position at Seoul National University, Korea.

Work

Kaang's studies have mainly focused on the molecular mechanisms of learning and memory. In his Ph.D. course, he developed the microinjection-based gene transfer method for Aplysia neurons. This technology opened up a new era of molecular studies on the memory mechanisms in Aplysia, as well as of functional studies of receptors, signaling molecules, and ion channels, which play key roles in neuronal functions. He revealed that serotonin-induced transcription requires the protein kinase-A-mediated phosphorylation of the cAMP-response element-binding protein (CREB). Moreover, he found that multiple pulses of serotonin stimulate gene expression that is mediated by the cAMP-response element (CRE). [1] [2]

He continued to study Aplysia when he set up his own laboratory in Korea. He started by establishing an expressed sequence tag database and transcriptome analyses of Aplysia. He identified a serotonin receptor involved in learning-related synaptic facilitation in Aplysia. In addition, he was successful in finding the novel signaling molecules ApLLP, CAMAP, ApPDE4, and ApAUF1, which are involved in long-term facilitation. With his colleagues at Columbia University, he delineated the molecular networks of the molecules that interplay with other regulatory molecules, such as ApCAM, CREB1, CREB2, C/EBP, and ApAF. Furthermore, Kaang reported that, by genetically controlling the expression of these key molecules in specific neurons, he could induce long-term facilitation that lasted days with a single pulse of serotonin that normally induces short-term facilitation that lasts only several minutes. [3] [4] [5] [6] [7] [8] [9] [10] [11]

In parallel with these studies in Aplysia, Kaang has expanded his research field to more complex mammalian models. Combining molecular, electrophysiological, and behavioral experimental tools, he began to explore the mechanisms of learning and memory in mice. One of the major findings from his group was proving the importance of synaptic protein degradation in memory reorganization. He found that postsynaptic proteins were degraded in the hippocampus by polyubiquitination after the retrieval of contextual fear memory. Moreover, the infusion of proteasome inhibitors into the CA1 of the hippocampus immediately after retrieval prevented anisomycin-induced memory impairment and the extinction of fear memory. Another major finding from his laboratory was the importance of a kinase, PI3Kγ, in long-term depression and behavioral flexibility. [12] [13] [14]

His interests also include neurological symptoms such as pain and itch and psychiatric disorders, such as autism. One of his major investigations regarding pain was proving that PKMζ, a molecule known for its role in the maintenance of long-term potentiation and long-term memory, is important in maintaining chronic pain in the anterior cingulate cortex. In collaboration with Min Zhuo from the University of Toronto, he showed that the phosphorylation of PKMζ was increased in a neuropathic pain model in the anterior cingulate cortex. In addition, they showed that chronic pain behavior was alleviated by treating mice with the PKMζ blocker ZIP, suggesting that this could be a new therapeutic target for treating chronic pain. [15] [16] [17] [18]

In collaboration with M.G. Lee and E. Kim, he demonstrated that NMDAR-dependent synaptic plasticity in the hippocampus is impaired in a mouse model of autism, the Shank2 knockout. When they treated the mice with drugs that upregulate NMDA receptor function, the impairment was recovered, suggesting the possibility that these drugs could be used for treating patients with autism in the future. [19]

Kaang has published 110 research and review articles in a number of journals, including Nature, Science, Cell, Neuron, and Nature Neuroscience. He has been the editor-in-chief of Molecular Brain. Kaang received the Life Science Award from the Korean Society for Molecular and Cellular Biology in 2008. He was awarded the Donghun Award from the Korean Society for Biochemistry and Molecular Biology in 2012. He also won the Kyung-Ahm Prize in the same year from the Kyung Ahm Foundation.

Awards

References

  1. ^ Kaang BK, Pfaffinger PI, Grant SG, Kandel ER, Furukawa Y (1992). "Overexpression of an Aplysia shaker K+channel gene modifies the electrical properties and synaptic efficacy of identified Aplysia neurons". Proc Natl Acad Sci USA. 89 (3): 1133–1137. Bibcode: 1992PNAS...89.1133K. doi: 10.1073/pnas.89.3.1133. PMC  48400. PMID  1310540.
  2. ^ Kaang BK, Kandel ER, Grant SG (1993). "Activation of cAMP-responsive genes by stimuli that produce long-term facilitation in Aplysia sensory neurons". Neuron. 10 (3): 427–435. doi: 10.1016/0896-6273(93)90331-k. PMID  8384857. S2CID  5520552.
  3. ^ Lee YS, Choi SL, Lee SH, Kim H, Park H, Lee N, Lee SH, Chae YS, Jang DJ, Kandel ER, Kaang BK (2009). "Identification of a serotonin receptor coupled to adenylyl cyclase involved in learning related heterosynaptic facilitation in Aplysia". Proc Natl Acad Sci USA. 106 (34): 14634–14639. Bibcode: 2009PNAS..10614634L. doi: 10.1073/pnas.0907502106. PMC  2732834. PMID  19706550.
  4. ^ Kim H, Lee SH, Han JH, Lee JA, Cheang YH, Chang DJ, Lee YS, Kaang BK (2006). "A nucleolar protein ApLLP induces ApC/EBP expression required for long-term synaptic facilitation in Aplysia neurons". Neuron. 49 (5): 707–718. doi: 10.1016/j.neuron.2006.01.035. PMID  16504946.
  5. ^ Lee SH, Lim CS, Park H, Lee JA, Han JH, Kim H, Cheang YH, Lee SH, Lee YS, Ko HG, Jang DH, Kim H, Miniaci MC, Bartsch D, Kim E, Bailey CH, Kandel ER, Kaang BK (2007). "Nuclear translocation of CAM-associated protein activates transcription for long-term facilitation in Aplysia". Cell. 129 (4): 801–812. doi: 10.1016/j.cell.2007.03.041. PMID  17512412.
  6. ^ Lee YS, Choi SL, Jun H, Yim SJ, Lee JA, Kim HF, Lee SH, Shim J, Lee K, Jang DJ, Kaang BK (2012). "AU-rich element-binding protein negatively regulates CCAAT enhancer-binding protein mRNA stability during long-term synaptic plasticity in Aplysia". Proc Natl Acad Sci USA. 109 (38): 15520–15525. Bibcode: 2012PNAS..10915520L. doi: 10.1073/pnas.1116224109. PMC  3458389. PMID  22949683.
  7. ^ Jang DJ, Park SW, Lee JA, Lee C, Chae YS, Park H, Kim MJ, Choi SL, Lee N, Kim H, Kaang BK (2010). "N termini of apPDE4 isoforms are responsible for targeting the isoforms to different cellular membranes". Learn Mem. 17 (9): 469–479. doi: 10.1101/lm.1899410. PMID  20813835.
  8. ^ Lee JA, Kim H, Lee YS, Kaang BK (2003). "Overexpression and RNA interference of Ap-cyclic AMP-response element binding protein-2, a repressor of long-term facilitation, in Aplysia kurodai sensory-to-motor synapses". Neurosci Lett. 337 (1): 9–12. doi: 10.1016/s0304-3940(02)01285-5. PMID  12524159. S2CID  17255313.
  9. ^ Lee JA, Kim HK, Kim KH, Han JH, Lee YS, Lim CS, Chang DJ, Kubo T, Kaang BK (2001). "Overexpression of and RNA interference with the CCAAT enhancer-binding protein on long-term facilitation of Aplysia sensory to motor synapses". Learn Mem. 8 (4): 220–226. doi: 10.1101/lm.40201. PMC  311377. PMID  11533225.
  10. ^ Lee JA, Lee SH, Lee CH, Chang DJ, Lee Y, Kim H, Cheang YH, Ko HG, Lee YS, Jun HJ, Bartsch D, Kandel ER, Kaang BK (2006). "PKA-activated ApAF-ApC/EBP heterodimer is a key downstream effector of ApCREB and is necessary and sufficient for the consolidation of long-term facilitation". J Cell Biol. 174 (6): 827–838. doi: 10.1083/jcb.200512066. PMC  2064337. PMID  16966424.
  11. ^ Lee YS, Bailey CH, Kandel ER, Kaang BK (2008). "Transcriptional regulation of long-term memory in the marine snail Aplysia". Mol Brain. 1: 3. doi: 10.1186/1756-6606-1-3. PMC  2546398. PMID  18803855.
  12. ^ Lee SH, Choi JH, Lee N, Lee HR, Kim JI, Yu NK, Choi SL, Lee SH, Kim H, Kaang BK (2008). "Synaptic Protein Degradation Underlies Destabilization of Retrieved Fear Memory". Science. 319 (5867): 1253–1259. Bibcode: 2008Sci...319.1253L. doi: 10.1126/science.1150541. PMID  18258863. S2CID  45611862.
  13. ^ Kaang BK, Lee SH, Kim H (2009). "Synaptic Protein Degradation as a Mechanism in Memory Reorganization". Neuroscientist. 15 (5): 430–435. doi: 10.1177/1073858408331374. PMID  19264729. S2CID  18724901.
  14. ^ Kim JI, Lee HR, Sim SE, Baek J, Yu NK, Choi JH, Ko HG, Lee YS, Park SW, Kwak C, Ahn SJ, Choi SY, Kim H, Kim KH, Backx PH, Bradley CA, Kim E, Jang DJ, Lee K, Kim SJ, Zhuo M, Collingridge GL, Kaang BK (2011). "PI3K is required for NMDAR-dependent long-term depression and behavioral flexibility". Nat Neurosci. 14 (11): 1447–1454. doi: 10.1038/nn.2937. PMID  22019731. S2CID  16198101.
  15. ^ Li XY; Ko HG; Chen T; Descalzi G; Koga K; Wang H; Kim SS; Shang Y; Kwak C; Park SW; Shim J; Lee K; Collingridge GL; Kaang BK*; Zhuo M.* (2010). "Alleviating neuropathic pain hypersensitivity by inhibiting PKMζ in the anterior cingulate cortex". Science. 330 (6009): 1400–1404. Bibcode: 2010Sci...330.1400L. doi: 10.1126/science.1191792. PMID  21127255. S2CID  5125595.
  16. ^ Lee B, Baek BJ, Deslcazi G, Kim JI, Lee HR, Lee K, Kaang BK, Zhuo M (2011). "Enhanced itch responses in mice lacking phosphoinositide 3-kinase-γ". Mol Pain. 7: 1744–8069–7–96. doi: 10.1186/1744-8069-7-96. PMC  3261823. PMID  22168443.
  17. ^ Kang SJ; Liu MG; Chen T; Ko HG; Baek GC; Lee HR; Lee K; Collingridge GL; Kaang BK*; Min Zhuo*. (2012). "Plasticity of metabotropic glutamate receptor dependent long-term depression in the ACC after amputation". J Neurosci. 32 (33): 11318–11329. doi: 10.1523/jneurosci.0146-12.2012. PMC  6621183. PMID  22895715.
  18. ^ Lee B, Baek BJ, Deslcazi G, Kim JI, Lee HR, Lee K, Kaang BK, Zhuo M (2011). "Enhanced itch responses in mice lacking phosphoinositide 3-kinase-γ" (PDF). Mol Pain. 7: 1744–8069–7–96. doi: 10.1186/1744-8069-7-96. PMC  3261823. PMID  22168443.
  19. ^ Won H; Lee HR; Gee HY; Mah W; Kim JI; Lee J; Ha S; Chung C; Jung ES; Cho YS; Park SG; Lee JS; Lee K; Kim D; Bae YC; Kaang BK*; Lee MG*; Kim E*. (June 2012). "Autistic-like social behaviour in Shank2-mutant mice improved by restoring NMDA receptor function". Nature. 486 (7402): 261–265. Bibcode: 2012Natur.486..261W. doi: 10.1038/nature11208. PMID  22699620. S2CID  4423977.
  20. ^ 원호섭 (25 June 2018). "최고과학기술인상에 강봉균·박진수". 매일경제 (in Korean). Retrieved 16 November 2023.

Publications

External links

Retrieved from " https://en.wikipedia.org/?title=Kaang_Bong-kiun&oldid=1223929645"

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