Endoplasmic Reticulum (ER) stress is associated with a variety of pathophysiological conditions, such as neurodegenerative diseases, diabetes, tumor growth under hypoxic conditions, and ischemic heart disease. Proteins in the ER misfold or unfold, and accumulate under stress conditions, which promote the expression of ER stress responsive genes. One of the mechanisms for mediating ER stress response is the activation of transcription factor ATF6. The quiescent form of ATF6 (p90ATF6), a type II-transmembrane protein, is embedded in the ER membrane and proteolyzed in an ER stress-dependent manner. The liberated N-terminal fragment (p50ATF6) translocates to the nucleus, binding to ER stress response element (ERSE) present in the proximal promoter regions of many ER stress-responsive proteins including ER chaperones. To better understand the pathological processes and provide novel avenues to potential therapies, ESRE–bla HeLa cells are engineered to express beta-lactamase under the control of ER stress response element. This is a clonal population isolated by FACS and its dose response curves with tunicamycin and thapsigargin are performed. This cell line also response to other known ER stress inducers.
For Research Use Only. Not for use in diagnostic procedures.
사양
대체 작용제
Thapsigargin
길항제
Salubrinal
어세이 입력
Cell-based beta lactamase reporter gene
셀 상태
Dividing Cells
검출 방법
Fluorescent
용도(애플리케이션)
FRET
유전자 기호
ESRE
인간 단백질 분류
Cell Signalling
일차 작용제
Tunicamycin
제품라인
CellSensor™
판독
End Point
리포터 유전자
BLA (Beta-Lactamase), BLA (Beta-lactamase)
타겟 입력
ATF6, ER stress response pathway
세포주
HeLa
System Type
CellSensor™
Druggable Target
Signaling Pathway
구성 및 보관
CellSensor™ ESRE-bla HeLa cells are shipped on dry ice. Store in liquid nitrogen immediately upon receipt, or thaw for immediate use.