ABL(유전자)

ABL (gene)
ABL1
사용 가능한 구조
PDBOrtholog 검색: PDBe RCSB
식별자
에일리어스ABL1, ABL 프로토온코제1, 비수용체 티로신인산화효소, ABL, JTK7, bcr/abl, c-ABL, c-p150, v-abl, CHDSKM, BCR-ABL, 유전자, ABL
외부 IDOMIM: 189980 MGI: 87859 HomoloGene: 3783 GeneCard: ABL1
EC 번호2.7.10.2
맞춤법
종.인간마우스
엔트레즈

25

11350

앙상블

ENSG000097007

ENSMUSG000026842

유니프로트

P00519

P00520

RefSeq(mRNA)

NM_007313
NM_005157

NM_001112703
NM_009594
NM_001283045
NM_001283046
NM_001283047

RefSeq(단백질)

NP_005148
NP_009297

NP_001106174
NP_001269974
NP_001269975
NP_001269976
NP_033724

장소(UCSC)Chr 9: 130.71 ~130.89 MbChr 2: 31.58 ~31.69 Mb
PubMed 검색[3][4]
위키데이터
인간 보기/편집마우스 표시/편집

Tyrosine-protein ABL1 또한 ABL1으로 알려져 있다. 단백질은, 인간의, ABL1 유전자(이전의 상징 축성협설면성의)염색체 9에 위치에 자리함로 인산화 효소.당초는 아벨 손 쥐 백혈병 비아이에서 분리 바이러스 유전자에 보내는 동안 v-Abl 말한다[5]c-Abl은 때때로 유전자의 버전을 포유류의 게놈 내에서 볼 수 있는 참조하는데 사용한다.러스[6]

기능.

ABL1 원형은 세포 분화, 세포 분열, 세포 접착 및 DNA [7][8][9][10]복구와 같은 스트레스 반응 과정에 관여된 세포질 및 핵 단백질 티로신 키나제를 암호화합니다.ABL1 단백질의 활성은 그 SH3 도메인에 의해 음성적으로 조절되며, SH3 도메인의 결실은 ABL1을 종양유전자로 변화시킨다.t(9;22) 전위는 BCR과 ABL1 유전자의 머리-꼬리 융합을 초래하여 많은 만성 골수성 백혈병 사례에서 존재하는 융합 유전자로 이어진다.보편적으로 발현되는 ABL1 티로신 인산화효소의 DNA 결합 활성은 CDC2 매개 인산화로 조절되어 ABL1의 세포 주기 기능을 시사한다.ABL1 유전자는 6kb 또는 [11]7kb mRNA 전사체로 발현되며, 대체적으로 공통 엑손 2-11에 스플라이싱된 첫 엑손이다.

임상적 의의

2세대 Bcr-Abl 티로신-키나아제 인히보르닐로티니브(빨간색)와 복합체 ABL1 키나아제 도메인

ABL1 유전자의 돌연변이는 만성 골수성 백혈병과 관련이 있다.CML에서 이 유전자는 염색체 22의 BCR(브레이크포인트 클러스터 영역) 유전자 내에 위치함으로써 활성화된다.이 새로운 융합 유전자 BCR-ABL은 조절되지 않은 세포질 표적 티로신 키나제를 암호화하여 세포들이 사이토카인에 의해 조절되지 않고 증식할 수 있게 합니다.이것은, 차례로, 세포를 암으로 만들 수 있게 한다.

이 유전자는 필라델피아 염색체의 BCR 유전자와 융합 유전자의 파트너로 만성 골수성 백혈병(CML)의 특징적인 이상이며 다른 백혈병 형태에서는 드물게 나타난다.BCR-ABL 전사는 티로신 키나제를 암호화하여 세포 주기 조절 시스템의 매개자를 활성화하여 클론 골수 증식 장애를 일으킨다.BCR-ABL 단백질은 다양한 작은 분자에 의해 억제될 수 있다.그러한 억제제 중 하나는 이미니브 메실레이트이며, 이는 티로신 키나아제 도메인을 차지하고 세포 사이클에 대한 BCR-ABL의 영향을 억제한다.이마티니브에 [12]내성을 가진 BCR-ABL 돌연변이를 억제하기 위한 2세대 BCR-ABL 티로신-키나아제 억제제도 개발 중이다.

상호 작용

ABL 유전자는 다음과 상호작용하는 것으로 나타났다.

규정

Abl의 발현이 microRNA miR-203에 [61]의해 조절된다는 증거가 있다.

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레퍼런스

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