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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, 69–72]

YY1

Positive and negative regulator of genes involved in biological processes such as differentiation, replication, and cellular proliferation.

Cancers, SLE, neurodegeneration

Stimulate

[73–76]

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, 77–80]

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

[86–90]