린

LYN
다른 용도는 Lyn(동음이의)을 참조하십시오.
린
PDB 1wa7 EBI.png
사용 가능한 구조물
PDB직교 검색: PDBe RCSB
식별자
별칭LIN, LIN 프로토-온세진, Src 계열 tyrosine kinase, JTK8, p53Lyn, p56Lyn
외부 IDOMIM: 165120 MGI: 96892 HomoloGene: 55649 GeneCard: LIN
직교체
종인간마우스
엔트레스

4067

17096

앙상블

ENSG00000254087

ENSMUSG00000042228

유니프로트

P07948

P25911

RefSeq(mRNA)

NM_001111097
NM_002350

NM_001111096
NM_010747

RefSeq(단백질)

NP_001104567
NP_002341

NP_001104566
NP_034877

위치(UCSC)Cr 8: 55.88 – 56.01MbChr 4: 3.68 – 3.81Mb
PubMed 검색[3][4]
위키다타
인간 보기/편집마우스 보기/편집

Tyrosine-단백질 kinase Lyn은 인간에서 LIN 유전자에 의해 암호화된 단백질이다.[5]

린은 주로 조혈모세포,[6] 신경조직간[7], 지방조직 등에서 발현되는 단백질 티로신키나제 src 계열의 일원이다.[8]각종 조혈모세포에서 린은 세포활성화 규제에 관여하는 핵심 효소로 떠올랐다.이들 세포에서 소량의 LIN은 B세포항원수용체(BCR),[9][10] CD40, [11]CD19 등 세포표면수용체 단백질과 연관된다.[12]약칭 Lyn은 Lck/Yes new tyrosine kinase, Lck, Yes도 Src kinase 계열의 구성원으로서 유래되었다.

함수

린은 골수성 혈통 증식에 억제적인 역할을 하고 있다고 묘사되어 왔다.[13]B세포 수용체의 결합에 따라 린은 빠른 인산화 및 활성화를 겪는다.LIN 활성화는 수용체 단백질의 면역수용체 타이로신 기반 활성화 모티브(ITAM) 내에서 타이로신 잔류물의 린인산화 작용에 의해 매개되는 신호 이벤트와 이후 Syk, Phosholipase C22(PLC22) 및 Phosphidyl inositol-3 kinase를 포함한 기타 키나제들의 모집 및 활성화에 의해 연쇄적으로 발생한다.[12][14]이러한 키나제들은 확산, Ca2+ 동원, 세포 분화에 중요한 역할을 하는 활성화 신호를 제공한다.린은 CD22, PIR-B, FCγRIIB1과 같은 규제 단백질에서 면역수용체 타이로신 기반 억제 모티브(ITIM) 내에서 타이로신 잔여물의 인산화(phosphylation)를 통한 억제 신호의 전송에 필수적인 역할을 한다.그들의 ITIM 인산염은 그 후 SHIP-1과 SHP-1과 같은 인산염의 모집과 활성화로 이어지고,[15][16][17][18][19] 이것은 신호 경로를 더욱 하향조정하고, 세포 활성화를 약화시키며, 내성을 중재할 수 있다.B세포에서 린은 세포 신호의 임계값을 설정하고 활성화와 억제 사이의 균형을 유지한다.따라서 린은 바이너리 온오프 스위치보다는 신호를 변조하는 루스태트로 기능한다.[20][21][22]HSP90 억제제 NVP-BEP800은 NF-kappaB 신호 억제를 통해 LIN 키나제의 안정성과 B세포 급성 림프탄성 백혈병의 성장에 영향을 미치는 것으로 설명되었다.[23]

인간 골성분화, 생존, 기능에 대한 에스트로겐 의존적 억제를 위한 핵심 신호 중재자가 LIN인 것으로 알려졌다.[24]린은 또한 인슐린 신호 전달 경로에 역할을 하는 것으로 연루되었다.활성 린인포릴레이트 인슐린 수용체 기질 1(IRS1)IRS1의 이러한 인산화 작용은 글루트-4의 세포막으로의 번역의 증가와 포도당 이용 증가로 이어진다.[25]결과적으로 인슐린 수용체의 활성화는 가능한 피드백 루프를 암시하는 린의 자기인산화를 증가시키는 것으로 나타났다.[26]인슐린 분비물인 글라이미피라이드(Amaryl®)는 지질 뗏목의 붕괴를 통해 아디프로모세포의 린을 활성화시킨다.[27]이 간접 Lyn 활성화는 글라임피라이드의 외부 생성 혈당 제어 활성을 변조할 수 있다.[27][28]톨리미돈(MLR-1023)은 EC50 63nM의[29][30] 린키나제의 소분자 알로스테리 활성제로 현재 제2형 당뇨병에 대한 2a단계 조사가 진행 중이다.[31]2016년 6월 이들 연구의 후원자인 멜리오르 디스커버리(Melior Discovery)는 당뇨병 환자들에게 톨리미돈(톨리미돈)을 투여한 Phase [32][33]2a 연구와 추가 임상연구의 지속을 통해 긍정적인 결과를 발표했다.[34]

린은 간세포탈출증으로부터 보호하고 간세포 미토콘드리아 무결성의 보존을 통해 간 재생을 촉진하는 것으로 나타났다.[35]

여러 조사관들이 폐 기능의 다른 측면들에서 린키나제의 역할을 보여주었다.폐상피에서 린 활성화가 폐장벽의 건전성을 향상시키고 부종을 줄이는 데 중요한 것으로 나타났다.[36][37]추가적인 증거는 폐포세포의 린 활성화가 박테리아의 혈소판을 개선하고 폐 감염을 감소시킨다는 것을 암시한다.[38][39] 마지막으로, 다른 연구들은 린 활성화가 점액의 폐의 과다 분비를 감소시킨다는 것을 발견했다.[40]


병리학

린에 대한 현재 지식의 대부분은 유전적으로 조작된 쥐에 대한 연구로부터 나왔다.린 결핍 생쥐는 골수성 종양과 골수성 종양의 급격한 증가인 비장상구균을 포함하는 표현형을 보여준다.이들 돌연변이의 세포에 대한 생화학적 분석 결과 린은 ITIM 의존적 억제 신호를 확립하고 골수세포 내 특정 단백질 타이로신인산염의 활성화를 위해 필수적이라는 사실이 밝혀졌다.[13]

과잉반응 린 알레르기를 발현한 생쥐는 종양이 없고 혈액학적 악성종양에 대한 성향이 전혀 보이지 않았다.이 생쥐들은 전통적인 B 림프구, 하향 조절 표면 면역글로불린 M과 비용 조절 분자의 수를 줄였고, B1a B 세포의 수를 증가시켰다.나이가 들면서 이 동물들은 기대수명의 30% 감소와 관련된 글루머루온염 표현형을 발달시켰다.[41]

상호작용

LIN은 다음과 상호 작용하는 것으로 나타났다.

참고 항목

참조

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