DNA damage-inducible transcript 4-like protein (DDIT4L)

DNA damage-inducible transcript 4-like protein (DDIT4L, also known as REDD2) is a small, regulatory protein encoded by the DDIT4L gene, in humans present on chromosome 4[1][3]. DDIT4L functions as a stress-responsive mTOR pathway inhibitor, activating in response to cellular stresses such as hypoxia and DNA damage, and negatively regulating cell growth by inhibiting the mTOR pathway primarily upstream of the TSC1-TSC2 complex and downstream of AKT1[3][6]. Elevated DDIT4L expression has been linked to increased autophagy, decreased mTORC1 activity, and roles in cell death, particularly under pathological or stress conditions in tissues such as the heart[1]. It is differentially expressed in certain cancers, where it may play either tumor suppressor or oncogenic roles depending on context and tissue type, and has been investigated as a biomarker in colorectal cancer, fibrosis, and hypertrophy[2][1]. No direct pharmacological modulators or drugs currently target DDIT4L itself, but it acts within the PI3K/AKT/mTOR signaling network relevant to therapeutic interventions in cancer and other diseases[2][3].

Other names

REDD2Rtp801LRegulated in development and DNA damage response 2DNA damage inducible transcript 4 likeRTP801LHIF-1 responsive protein RTP801-likeProtein regulated in development and DNA damage response 2Similar to Smhs1 proteinHomolog of mouse SMHS1