ArticleMolecular and cellular endocrinology2013
AXL and MET crosstalk to promote gonadotropin releasing hormone (GnRH) neuronal cell migration and survival.
Article in Molecular and cellular endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 50 citations in OpenAlex.
- C-MET tyrosine kinase receptor: mechanisms, clinical applications and future perspectives in cancer therapy.Signal transduction and targeted therapy · 2026Review
- Recent Advances in the Understanding of Gonadotrope Lineage Differentiation in the Developing Pituitary.Neuroendocrinology · 2025Review
- AXL as immune regulator and therapeutic target in Acute Myeloid Leukemia: from current progress to novel strategies.Experimental hematology & oncology · 2024Review
- Identifying Qingkailing ingredients-dependent mesenchymal-epithelial transition factor-axiation "π" structuring module with angiogenesis and neurogenesis effects.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- PFKP silencing suppresses tumor growth via the AXL-MET axis.International journal of biological sciences · 2024Article
- Targeting HER2-AXL heterodimerization to overcome resistance to HER2 blockade in breast cancer.Science advances · 2022Article
- Review
- Preclinical characterization and phase I clinical trial of CT053PTSA targets MET, AXL, and VEGFR2 in patients with advanced solid tumors.Frontiers in immunology · 2022Article
- Role of p38 MAPK Signalling in Testis Development and Male Fertility.Oxidative medicine and cellular longevity · 2022Review
- Review
- Control of cortical synapse development and plasticity by MET receptor tyrosine kinase, a genetic risk factor for autism.Journal of neuroscience research · 2020Review
- Review
- MET targeting: time for a rematch.Oncogene · 2020Review
- AXL as a Target in Breast Cancer Therapy.Journal of oncology · 2020Review
- Gas6 expression is reduced in advanced breast cancers.NPJ precision oncology · 2020Article
- HGF/c-Met Axis: The Advanced Development in Digestive System Cancer.Frontiers in cell and developmental biology · 2020Review
- The RTK Interactome: Overview and Perspective on RTK Heterointeractions.Chemical reviews · 2019Review
- The Relationships Between Vitamin K and Cognition: A Review of Current Evidence.Frontiers in neurology · 2019Review
- AXL phosphorylates and up-regulates TNS2 and its implications in IRS-1-associated metabolism in cancer cells.Journal of biomedical science · 2018Article
- HGF-induced formation of the MET-AXL-ELMO2-DOCK180 complex promotes RAC1 activation, receptor clustering, and cancer cell migration and invasion.The Journal of biological chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The membrane tyrosine kinase receptors, AXL and MET, are implicated in GnRH neuron migration and/or survival. We hypothesized that the receptors with their ligands, GAS6 and HGF, respectively may cross-talk in GnRH neuronal function. In NLT GnRH neuronal cells, MET co-immunoprecipitated with AXL, although HGF or GAS6 did not transphosphorylate AXL or MET, respectively. Co-expression of a kinase dead AXL blocked HGF activation of MET and indirectly AKT and p38MAPK. Silencing of AXL decreased HGF's ability to phosphorylate MET and activate AXL's downstream effectors, p38MAPK and AKT. HGF/MET signaling modulated neuron migration dependent and independent of AXL co-expression and p38MAPK. Conversely, AXL's control of GnRH neuronal survival was dependent on HGF/MET signaling. Together, these data support that the importance of membrane tyrosine kinase receptor crosstalk to regulate neuronal cell-specific developmental functions.
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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.