ReviewCold Spring Harbor perspectives in biology2013
Molecular mechanisms of SH2- and PTB-domain-containing proteins in receptor tyrosine kinase signaling.
Review in Cold Spring Harbor perspectives in biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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
89 citing papers in PubMed.
- Preclinical in vitro and in vivo activity of trastuzumab deruxtecan againstGynecologic oncology reports · 2026Article
- Structure-based identification, phosphorylation, cyclization and engineering of a self-binding peptide carboxy-terminal to EGFR kinase domain by integrating dynamics simulation, energetics calculation and fluorescence analysis.European biophysics journal : EBJ · 2026Article
- Tyrosine Kinase Receptors, Inhibition, and Potential Role in the Pharmacotherapy of Retinal Disorders.Ophthalmology and therapy · 2026Review
- Regulation of CFTR stability at the plasma membrane-Mechanisms and therapeutic opportunities in cystic fibrosis.FEBS letters · 2026Review
- Decoding C‑SH2 Domain/Peptide Interactions in SH2 Domain-Containing Tyrosine Phosphatase 2: A Molecular Framework for Rational Inhibitor Design.ACS omega · 2026Article
- DCBLD1 Promotes Lung Tumorigenesis by Inhibiting PTP1B Dephosphorylation of EGFR.International journal of biological sciences · 2026Article
- Unraveling novel mechanisms of ATP-Binding cassette (ABC) transporter in insulin Resistance-induced amyloidogenesis.Metabolic brain disease · 2025Review
- Unraveling the Mystery of Insulin Resistance: From Principle Mechanistic Insights and Consequences to Therapeutic Interventions.International journal of molecular sciences · 2025Review
- Growth hormone signaling and clinical implications: from molecular to therapeutic perspectives.Molecular biology reports · 2025Review
- Transcripts from themicroPublication biology · 2025Article
- Article
- Article
- The Evolving Paradigm of Antibody-Drug Conjugates Targeting the ErbB/HER Family of Receptor Tyrosine Kinases.Pharmaceutics · 2024Review
- Transmembrane helix interactions regulate oligomerization of the receptor tyrosine kinase EphA2.The Journal of biological chemistry · 2024Article
- GRB2 stabilizes RAD51 at reversed replication forks suppressing genomic instability and innate immunity against cancer.Nature communications · 2024Article
- Crosstalk between KDEL receptor and EGF receptor mediates cell proliferation and migration via STAT3 signaling.Cell communication and signaling : CCS · 2024Article
- Docking protein 6 (DOK6) selectively docks the neurotrophic signaling transduction to restrain peripheral neuropathy.Signal transduction and targeted therapy · 2024Article
- The pathogen-encoded signalling receptor Tir exploits host-like intrinsic disorder for infection.Communications biology · 2024Article
- Review
- Article
29 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular signaling is mediated by reversible posttranslational modifications (PTMs) that include phosphorylation, ubiquitination, and acetylation, among others. In response to extracellular stimuli such as growth factors, receptor tyrosine kinases (RTKs) typically dimerize and initiate signaling through phosphorylation of their cytoplasmic tails and downstream scaffolds. Signaling effectors are recruited to these phosphotyrosine (pTyr) sites primarily through Src homology 2 (SH2) domains and pTyr-binding (PTB) domains. This review describes how these conserved domains specifically recognize pTyr residues and play a major role in mediating precise downstream signaling events.
Indexed as
Identifiers
What Socratic 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 Socratic graph.