Luokat: Kaikki - inflammation - migration - cancer - phosphorylation

jonka yu ho 12 vuotta sitten

467

shp2

The text details the intricate interactions and pathways involving various proteins and molecules in cellular processes. It highlights the role of SHP2 and its influence on different signaling pathways, including JAK/

shp2

ERK1/2

C-myc

JAK/STAT instomach cancer

Gab1-p(BTAM)

CBP/PAG

IRS-1

IGF-1 자극시

IRS-1 pY895의 탈인산화 by SHP2

Src(active)

pY 416 - increae activity

pY 527 - decrease activity

IL-6

MAPK pathway

ERK1/2-p

= MAPK

; JAK 억제도 가능함

integrin/GF/GPCR

proliferation

AT1

SHP2 -P 되고 AT-1 옆에 위치

AT-1 JAK2 연결

sos

Src-p(inactive)

p-CBP/PAG

Gab2

Grb2

Rho family

RhoA

focal adhesion

Rac

assembly, protrusion

Cdc42

polarity, filopodia extention

RAS

VAV

inflammation

INF---->autophagy

이과정의 차단은 ROS 증가 shp2 증가 암을 유발.

antiproliferation

gp130

DAK1

insulin receptor substrate familyprotein

인테그린과 shp2연결

beta3 integrin

Gab1

-shp2

- PI3K 에 의해 인산화 PH domain

- PLCg

-Ras-GAP

all these protein SH2- 의해 Gab1 연결.

cell migration

STAT-P

JAK

CAG PATHWAY 에서는 NEGATIVE REGULATOR

Ang2 에서는 at연관 positive regulator

paxilin

adaptor protein

direct association with the cytoplasmic tail of beta-integrin

N-terminal region of paxillin is rich in protein–protein interaction sites

p-paxinlin

IN NUCLEUS DIMER TY 전사 조절

shp2

조직별 발현 차이 ; 간 신장 적게 발현

혈관 손상후 발현 증가.

노인에서 발현과 인산화 정도 증가

FAK

non receptor Y kinase

SHP2의 의해 주기적 활성/비활성 전환

Y397 에 탈인산화 SHP2와 직접 결합

PDGF

SHP2-phosphorylation (active)

pY1007in PDGF Receptor bind and dephosphorylate

PPAR

Rho 억제기능, shp2 활성 증대

shp2가 VAV( Rho kinase) 억제

EGFR

ANGIOTENSN 2

ROS

PTK

CAG A

as adaptor SHP2를 gp130으로

CAG A -p ; SHP2 binding 증가 ERK ERK-p 증가 염증증가

CAG A ; JAK/STAT 활성 증가 adenoma

by Src family of kinase

Subtopic
ulcer,gc