Skip to main content

Table 2 Transcription factors which have been experimentally shown to influence ERVK LTR activity

From: Endogenous retrovirus-K promoter: a landing strip for inflammatory transcription factors?

Transcription factor Cellular function Implicated diseases Effect on ERVK LTR References
Sp-1, Sp-3 Implicated in the regulation of genes that control multiple cellular processes, including cell cycle, apoptosis, and DNA damage. ALS, SLE, RA Alzheimer’s Disease, Huntington’s Disease Stimulate [22, 6972]
YY1 Positive and negative regulator of genes involved in biological processes such as differentiation, replication, and cellular proliferation. Cancers, SLE, neurodegeneration Stimulate [7376]
NF-kB Involved in cytoplasmic/nuclear signalling in response to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens; activates transcription of a variety of genes encoding immunologically relevant proteins. HIV infection, ALS, SLE, MS, Rheumatic disease, Cancers Stimulate [17, 69, 7780]
NFAT-1 Plays a key role in the regulation of cytokine gene transcription during the immune response. HIV infection, Alzheimer’s Disease, Autoimmune diseases Stimulate [17, 81, 82]
MITF-M Induces genes essential for melanin synthesis, melanosome formation, cell cycle progression, and cell survival; essential for development of retinal pigmented epithelium and neural crest derived melanocytes. Melanoma Stimulate [23]
PR Mediates the effects of progesterone on mammary gland development. Breast cancer Stimulate [83, 84]
ER Mediates the effects of estrogen on reproductive organs, bone, and brain. SLE, Breast cancer Stimulate [83, 85]
AR Mediates embryonic sexual differentiation and required for maintenance of spermatogenesis Prostate cancer, breast cancer, Kennedy’s disease Stimulate [8690]