ReviewSeminars in cancer biology2020
ITCH as a potential therapeutic target in human cancers.
Review in Seminars in cancer biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 61 citations in OpenAlex.
- CHFR drives gastric cancer stemness and hepatic metastasis by suppressing ITCH-mediated ubiquitination and degradation of OCT4.Biology direct · 2026Article
- The E3 ubiquitin ligase Itch plays an essential role in kidney fibrosis by inhibiting Dvl2/GSK3β/β-catenin signaling pathway.Cell death and differentiation · 2026Article
- MAML1 drives Notch and Hedgehog oncogenic pathways by inhibiting Itch activity in triple-negative breast cancer.Cell death and differentiation · 2026Article
- CD47 stabilizes ROBO2 to regulate glioblastoma progression by preventing ITCH-mediated ubiquitination.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- From Single-Cell Clusters to Causality: ITCH Engagement for CKD Uncovered by Integrative Analysis of MR and MAGMA.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- ALIX and ITCH localize to the base of primary cilia and negatively regulate ciliary Polycystin-2 levels.BMC molecular and cell biology · 2026Article
- Upregulation of itchy E3 ubiquitin protein ligase contributes to endometrial cancer through promoting forkhead box P1 degradation.CytoJournal · 2026Article
- The Crosstalk Between CRL5 and APC/C E3 Ligases Regulates Metastasis and Chemosensitivity of Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- E3 ubiquitin ligases in neurodegenerative diseases.Military Medical Research · 2026Review
- NX-1607: lifting the Cbl-b brake to promote T cell activation through MAPK/ERK pathways.Journal for immunotherapy of cancer · 2025Article
- Oxidative stress triggers Itch-mediated TXNIP degradation and NF-κB activation promoting chronic obstructive pulmonary disease.Respiratory research · 2025Article
- A structurally informed human protein-protein interactome reveals proteome-wide perturbations caused by disease mutations.Nature biotechnology · 2025Article
- RIPK2 promotes colorectal cancer metastasis by protecting YAP degradation from ITCH-mediated ubiquitination.Cell death & disease · 2025Article
- Possible Trace of HTLV-1 Virus in Modulation of Cbl-b, ITCH, and PP2A Suppressor Genes.International journal of molecular and cellular medicine · 2025Article
- Natural lung-tropic TJournal for immunotherapy of cancer · 2024Article
- Leveraging ancient DNA to uncover signals of natural selection in Europe lost due to admixture or drift.Nature communications · 2024Article
- Addressing the mean-variance relationship in spatially resolved transcriptomics data withbioRxiv : the preprint server for biology · 2024Article
- Article
- Targeting Intracranial Tumours with a Combination of RNA and Chemotherapy.Pharmaceutics · 2024Article
- The E3 ubiquitin ligase ITCH negatively regulates intercellular communication via gap junctions by targeting connexin43 for lysosomal degradation.Cellular and molecular life sciences : CMLS · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The ITCH/AIP4 ubiquitin E3 ligase was discovered independently by two groups searching for atrophin-1 interacting proteins and studying the genetics of mouse coat color alteration, respectively. ITCH is classified as a NEDD4 family E3 ligase featured with the C-terminal HECT domain for E3 ligase function and WW domains for substrate recruiting. ITCH deficiency in the mouse causes severe multi-organ autoimmune disease. Its roles in maintaining a balanced immune response have been extensively characterized over the past two and a half decades. A wealth of reports demonstrate a multifaceted role of ITCH in human cancers. Given the versatility of ITCH in catalyzing both proteolytic and non-proteolytic ubiquitination of its over fifty substrates, ITCH's role in malignancies is believed to be context-dependent. In this review, we summarize the downstream substrates of ITCH, the functions of ITCH in both tumor cells and the immune system, as well as the implications of such functions in human cancers. Moreover, we describe the upstream regulatory mechanisms of ITCH and the efforts have been made to target ITCH using small molecule inhibitors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.