4.4 Article

Regulation of major histocompatibility complex class I molecule expression on cancer cells by amyloid precursor-like protein 2

期刊

IMMUNOLOGIC RESEARCH
卷 51, 期 1, 页码 39-44

出版社

HUMANA PRESS INC
DOI: 10.1007/s12026-011-8238-6

关键词

Amyloid precursor-like protein 2; Antigen presentation; Cancer; Endocytosis; Major histocompatibility complex class I molecule; Human leukocyte antigen; Tumor antigen; Tumor immunology; Trafficking

资金

  1. NIH [P50CA127297, GM57428, GM74876, GM87455, T32 CA009476]
  2. NIH/NCRR COBRE [P20RR018759]
  3. ARRA Nebraska Center for Cellular Signaling Developmental Research
  4. Nebraska Dept. of Health and Human Services
  5. Nebraska Center for Cellular Signaling
  6. UNMC
  7. American Heart Association
  8. Graduate Assistance in Areas of National Need Fellowship
  9. NIH Cancer Center [P30CA036727]

向作者/读者索取更多资源

The three members of the amyloid precursor protein family in mammals [amyloid precursor protein, amyloid precursor-like protein 1, and amyloid precursor-like protein 2 (APLP2)] have been implicated in a large array of intracellular processes, which include development, transcription, apoptosis, metabolism, and the cell cycle. A series of studies by our laboratories has demonstrated that APLP2 is highly expressed by many cancer cell lines (with the highest expression in pancreatic cancer cell lines) and that it facilitates major histocompatibility complex (MHC) class I molecule endocytosis. This review focuses on this recently revealed function of APLP2 relevant to tumor immunology: that it acts as a novel regulator of MHC class I molecule surface expression.

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