핵인자 카파비

NF-κB의 작용 메커니즘. Rel과 p50 단백질로 구성된 NF-κB 이형이합체(heterodimer)의 작용에 관한 예시. 비활성 상태에서 NF-κB는 억제성 단백질인 IκBα와 결합한 상태로 세포질에 위치한다. 내재성 막단백질에 해당하는 수용체를 매개로 다양한 세포 외 신호가 IκB 키나아제(IKK)를 활성화 시킬 수 있다. IKK는 IκBα 단백질을 인산화시키고, 이어서 IκBα의 유비퀴틴화와 NF-κB에서의 탈부착, 프로테아좀에 의한 IκBα의 최종적인 분해를 초래한다. 억제성 단백질과 해리된 NF-κB는 활성화된 상태로 핵으로 이동하여 반응요소(response element, RE)라고하는 특정 DNA 서열에 결합한다. 이어서 DNA/NF-κB 복합체는 보조활성자와 RNA 폴리머레이즈와 같은 다른 단백질을 동원하여 하류 영역의 DNA 서열을 mRNA로 전사시킨다. mRNA는 단백질로 번역되어 세포 기능의 변화를 일으킨다.[1][2][3]
NF-κB 단백질의 구조. NF-κB 단백질은 크게 두 가지 구조적 클래스인 클래스 I(위)과 클래스 II(아래)로 구분할 수 있다. 둘 모두 N 말단의 DNA결합역(DNA Binding Domain, DBD)을 가지고 있다. 이 부위는 다른 NF-κB 전사인자와 이량체를 이룰 때 접합부위로 작용하며, 억제성 단백질인 IκBα의 결합부위이기도 하다. 클래스 I NF-κB 단백질의 C 말단은 안키린 반복 구조를 포함하고 있으며, 전사 억제 역할을 할 수 있다. 반면 클래스 II NF-κB 단백질의 C 말단은 전사 활성 기능을 가진다.[1][2][3]

핵인자 카파비(NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells)는 DNA의 전사 과정, 사이토카인의 생성과 세포의 생존에 관여하는 단백질 복합체이다. NF-κB는 거의 모든 동물 세포 종류에서 발견되며 다양한 자극에 대한 세포 반응, 예를 들어 스트레스, 사이토카인, 자유 라디칼, 중금속, 자외선 노출, 산화된 지방질, 박테리아 및 바이러스 항원 등에 대한 반응에 관여한다.[1][2][3][4][5]

NF-κB는 염증 반응에서 중요한 역할을 수행한다. NF-κB의 잘못된 전사 조절은 암, 염증성 질환과 자가면역질환, 패혈증 쇼크, 바이러스 감염, 면역계의 발달이상 등을 초래한다. NF-κB는 또한 시냅스 가소성 및 기억의 형성 과정에도 관여하는 것으로 알려져 있다.[6][7][8][9][10][11]

같이 보기

각주

  1. ↑ 가 나 다 Gilmore TD (October 2006). “Introduction to NF-κB: players, pathways, perspectives”. 《Oncogene》 25 (51): 6680–4. doi:10.1038/sj.onc.1209954. PMID 17072321. 
  2. ↑ 가 나 다 Brasier AR (2006). “The NF-κB regulatory network”. 《Cardiovascular Toxicology》 6 (2): 111–30. doi:10.1385/CT:6:2:111. PMID 17303919. 
  3. ↑ 가 나 다 Perkins ND (January 2007). “Integrating cell-signalling pathways with NF-κB and IKK function”. 《Nature Reviews Molecular Cell Biology》 8 (1): 49–62. doi:10.1038/nrm2083. PMID 17183360. 
  4. ↑ Gilmore TD (November 1999). “The Rel/NF-κB signal transduction pathway: introduction”. 《Oncogene》 18 (49): 6842–4. doi:10.1038/sj.onc.1203237. PMID 10602459. 
  5. ↑ Tian B, Brasier AR (2003). “Identification of a nuclear factor κB-dependent gene network”. 《Recent Progress in Hormone Research》 58: 95–130. doi:10.1210/rp.58.1.95. PMID 12795416. 
  6. ↑ Albensi BC, Mattson MP (February 2000). “Evidence for the involvement of TNF and NF-κB in hippocampal synaptic plasticity”. 《Synapse》 35 (2): 151–9. doi:10.1002/(SICI)1098-2396(200002)35:2<151::AID-SYN8>3.0.CO;2-P. PMID 10611641. 
  7. ↑ Meffert MK, Chang JM, Wiltgen BJ, Fanselow MS, Baltimore D (October 2003). “NF-κB functions in synaptic signaling and behavior” (PDF). 《Nature Neuroscience》 6 (10): 1072–8. doi:10.1038/nn1110. PMID 12947408. 
  8. ↑ Levenson JM, Choi S, Lee SY, Cao YA, Ahn HJ, Worley KC, Pizzi M, Liou HC, Sweatt JD (April 2004). “A bioinformatics analysis of memory consolidation reveals involvement of the transcription factor c-rel”. 《The Journal of Neuroscience》 24 (16): 3933–43. doi:10.1523/JNEUROSCI.5646-03.2004. PMID 15102909. 
  9. ↑ Freudenthal R, Locatelli F, Hermitte G, Maldonado H, Lafourcade C, Delorenzi A, Romano A (February 1998). “κ-B like DNA-binding activity is enhanced after spaced training that induces long-term memory in the crab Chasmagnathus”. 《Neuroscience Letters》 242 (3): 143–6. doi:10.1016/S0304-3940(98)00059-7. PMID 9530926. 
  10. ↑ Merlo E, Freudenthal R, Romano A (2002). “The IκB kinase inhibitor sulfasalazine impairs long-term memory in the crab Chasmagnathus”. 《Neuroscience》 112 (1): 161–72. doi:10.1016/S0306-4522(02)00049-0. PMID 12044481. 
  11. ↑ Park HJ, Youn HS (March 2013). “Mercury induces the expression of cyclooxygenase-2 and inducible nitric oxide synthase”. 《Toxicology and Industrial Health》 29 (2): 169–74. doi:10.1177/0748233711427048. PMID 22080037. 

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