ReviewCell communication and signaling : CCS2017
The Id-protein family in developmental and cancer-associated pathways.
Review in Cell communication and signaling : CCS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.
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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
134 citing papers in PubMed, 1 synthesis or guideline pooled it, 223 citations in OpenAlex.
- Milk-Derived Proteins and Peptides in Head and Neck Carcinoma Treatment.Biomolecules · 2022Pooled it
- The DCBLD2 super-enhancer drives colorectal cancer progression through FOSL2/JUND-mediated activation of the CD146/AKT/TNFRSF6B pathway.Molecular biomedicine · 2026Article
- Therapeutic target exploration of Shugan Jianpi formula in liver fibrosis: an integrated lncRNA-mRNA co-expression network analysis.Molecular genetics and genomics : MGG · 2026Article
- A working model for CCN3 C-terminal domain-mediated transcriptional modulation of the plasminogen activation system.Journal of cell communication and signaling · 2026Review
- ATOH1 and NPAS1 are immune related prognostic biomarkers in colorectal cancer.Discover oncology · 2026Article
- Harnessing Id1 as a biomarker in a plasmid reporter system for cervical cancer.Scientific reports · 2026Article
- Chemotherapy Enrichment of ID Family Expression Is Associated with IL-6 Signaling in Ovarian Cancer.Cancers · 2026Article
- USP35 Acts as a Deubiquitinating Enzyme for ID3 to Promote Immune Escape in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A novel spliceosomopathy caused by de novo SF3B3 variants.Genome medicine · 2026Article
- Molecular Signatures of Id2- and Ascl4-Induced Wiring of Adult Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- SMURF2 in Anticancer Therapy: Dual Role in Carcinogenesis and Theranostics.International journal of molecular sciences · 2026Review
- Integrative Multi-Omics and Machine Learning Identify ID1 as a Candidate Gene Associated with Abdominal Aortic Aneurysm.Current issues in molecular biology · 2026Article
- A prevalent disease-associated SNP in the humanNAR molecular medicine · 2026Article
- Simultaneous inhibition of ID1 and ID3 mitigates fibroblast activation via cell cycle and MEK/ERK pathways in pulmonary fibrosis.Theranostics · 2026Article
- Distinct transcriptional regulation of the Wnt and TGFβ signaling families associated with wound healing and fibrotic outcomes to lens injury.Experimental eye research · 2025Article
- Effects of Imposed Defocus on Inhibitor of DNA-Binding Gene Expression in Chick Posterior Ocular Tissues.Cells · 2025Article
- Targeting Ischemic Stroke with Neural Stem Cells: Insights into Endogenous Repair Mechanisms, Biomaterial-Based Delivery, and Exosome Therapies.Molecular neurobiology · 2025Review
- ID1 in hematopoiesis and hematologic disorders: novel potentials of a classic differentiation regulator.Cellular & molecular biology letters · 2025Review
- Helicobacter pylori-induced aberrant methylation of ID4 mediated by DNMT3B drives gastric cancer progression via DEC1-SHH signaling pathway.Cell death & disease · 2025Article
- Inhibitor of DNA binding-1 is a key regulator of cancer cell vasculogenic mimicry.Molecular oncology · 2025Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibitors of DNA binding and cell differentiation (Id) proteins are members of the large family of the helix-loop-helix (HLH) transcription factors, but they lack any DNA-binding motif. During development, the Id proteins play a key role in the regulation of cell-cycle progression and cell differentiation by modulating different cell-cycle regulators both by direct and indirect mechanisms. Several Id-protein interacting partners have been identified thus far, which belong to structurally and functionally unrelated families, including, among others, the class I and II bHLH transcription factors, the retinoblastoma protein and related pocket proteins, the paired-box transcription factors, and the S5a subunit of the 26 S proteasome. Although the HLH domain of the Id proteins is involved in most of their protein-protein interaction events, additional motifs located in their N-terminal and C-terminal regions are required for the recognition of diverse protein partners. The ability of the Id proteins to interact with structurally different proteins is likely to arise from their conformational flexibility: indeed, these proteins contain intrinsically disordered regions that, in the case of the HLH region, undergo folding upon self- or heteroassociation. Besides their crucial role for cell-fate determination and cell-cycle progression during development, other important cellular events have been related to the Id-protein expression in a number of pathologies. Dysregulated Id-protein expression has been associated with tumor growth, vascularization, invasiveness, metastasis, chemoresistance and stemness, as well as with various developmental defects and diseases. Herein we provide an overview on the structural properties, mode of action, biological function and therapeutic potential of these regulatory proteins.
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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.