Krueppel-like factor 10 (KLF10)

Krueppel-like factor 10 (KLF10) is a zinc finger transcription factor belonging to the Krueppel-like family and is rapidly induced by transforming growth factor-beta (TGFβ), estrogen, bone morphogenetic proteins, and other cytokines[1]. KLF10 functions primarily as a transcriptional regulator by binding to GC-rich Sp1-like DNA sequences, where it can activate or repress target gene expression. It plays a significant role in the TGFβ/Smad signaling pathway, contributing to the inhibition of cell proliferation, induction of apoptosis, and regulation of differentiation processes, especially in bone and immune cells[1][2]. KLF10 has been identified as a tumor suppressor in breast cancer and is critical for normal bone formation, osteoblast and osteoclast differentiation, and immune system homeostasis. Knockout studies in mice demonstrate effects on bone density, cardiac structure, tendon function, and immune responses, underscoring its broad physiological importance[1]. KLF10 is also involved in circadian and metabolic pathways through its transcriptional regulatory networks[2]. While it is not currently the direct target of any approved drugs, it is highly relevant to disease mechanisms, especially in cancer, bone disorders, cardiovascular disease, and immune-mediated processes[1][2].

Other names

TIEGTIEG1Transforming growth factor-beta-inducible early growth response protein 1early growth response alpha (EGR-alpha)EGRAzinc finger transcription factor TIEGEGRαTGFβ-inducible early gene-1

Modulation of gene expression via DNA-binding to GC-rich Sp1-like sequences, Regulation of TGFβ/Smad signaling, Repression of inhibitory Smad7, Activation of Smad2, Modulation of estrogen response, Immune response regulation via AhR–KLF10 axis