Affinage

RASAL2

Ras GTPase-activating protein nGAP · UniProt Q9UJF2

Length
1139 aa
Mass
128.6 kDa
Annotated
2026-06-10
39 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RASAL2 is a Ras GTPase-activating protein that catalyzes hydrolysis of Ras-GTP to restrain Ras-ERK signaling, functioning predominantly as a tumor and metastasis suppressor whose loss constitutes an alternative route to Ras hyperactivation in cancer (PMID:24029233). Through its catalytic suppression of Ras-ERK output, RASAL2 limits EMT, migration, invasion, and cancer stemness across ovarian and bladder tumors, with the latter mediated through a MAPK/SOX2 axis (PMID:25216515, PMID:28182001), and it further suppresses AKT-driven angiogenic programs by lowering ETS1/VEGFA and by activating GSK3β to reduce c-FOS/VEGFA (PMID:29702203, PMID:30158581). RASAL2 displays striking context-dependent duality: in triple-negative breast cancer it acts independently of GAP catalysis by binding and antagonizing the RAC1-GAP ARHGAP24 to activate RAC1 and drive mesenchymal invasion (PMID:25384218), while in gastric cancer it is induced by NF-κB and binds and inhibits PP2A to activate AKT and β-catenin (PMID:35134322); in colorectal, prostate, and pancreatic cancers it variously promotes proliferation and progression via nuclear translocation, AKT/cyclin D1 signaling, and YAP1/TIAM1 stabilization (PMID:31288861, PMID:35668070, PMID:35844783). Its activity is governed by AMPKα (PRKAA) phosphorylation at Ser351, which switches RASAL2 between a PPM1B-recruiting autophagy suppressor and an activator of the PIK3C3/VPS34-ATG14-BECN1 complex (PMID:33563064), and its abundance is controlled by CAMSAP2-driven ubiquitin-proteasome degradation (PMID:38159595). A germline RASAL2 p.Y808C variant enhances Ras signaling and confers resistance to anti-EGFR therapy (PMID:40849341).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2012 Medium

    Established that RASAL2 is not solely a Ras regulator but also engages Rho-family signaling, by identifying a physical link to the RhoGEF ECT2 controlling migratory plasticity.

    Evidence ECT2 immunoprecipitation/mass spectrometry, RHO activity assay, and RNAi phenotyping in astrocytoma cells

    PMID:22683310

    Open questions at the time
    • Direct vs. indirect nature of the RASAL2-ECT2 association not resolved by reciprocal validation
    • Connection between ECT2 binding and GAP catalysis unclear
  2. 2013 High

    Defined RASAL2 as a RasGAP tumor and metastasis suppressor in vivo, answering whether its loss is sufficient to hyperactivate Ras in cancer.

    Evidence Knockout mouse models, in vivo tumor/metastasis assays, and human breast cancer mutation/expression analysis

    PMID:24029233

    Open questions at the time
    • Structural basis of Ras-GTP hydrolysis not defined
    • Did not address context-specific oncogenic roles
  3. 2014 High

    Revealed that RASAL2 has a GAP-independent oncogenic mode, by showing it antagonizes the RAC1-GAP ARHGAP24 to activate RAC1 in TNBC.

    Evidence Reciprocal Co-IP, RAS-GAP catalytic mutant rescue, and RAC1 activity assays in TNBC cells

    PMID:25384218

    Open questions at the time
    • Determinants of whether RASAL2 acts as GAP or RAC1 activator in a given tumor unresolved
    • ARHGAP24 binding interface not mapped
  4. 2014 Medium

    Confirmed RASAL2 suppresses Ras-ERK-driven EMT in ovarian cancer via pharmacological epistasis.

    Evidence shRNA knockdown, migration/invasion assays, and ERK pathway inhibitor rescue

    PMID:25216515

    Open questions at the time
    • Single-lab evidence
    • Direct GAP substrate engagement not shown biochemically
  5. 2017 Medium

    Extended tumor-suppressor function to bladder cancer stemness through a defined MAPK/SOX2 axis, and to adipocyte biology where RASAL2 represses Ras in an ERK-independent manner.

    Evidence Gain/loss-of-function with ERK inhibitor and SOX2 siRNA rescue in bladder cancer; Rasal2-deficient mice and 3T3-L1 knockdown with Ras/MEK inhibitor rescue for adipogenesis

    PMID:28182001 PMID:28580280

    Open questions at the time
    • ERK-independent effector downstream of Ras in adipogenesis unidentified
    • Mechanism linking MAPK to SOX2 not fully resolved
  6. 2018 Medium

    Mapped distinct anti-angiogenic and oncogenic effector branches, placing RASAL2 upstream of AKT/ETS1/VEGFA and GSK3β/c-FOS/VEGFA in suppressor contexts and upstream of LATS2/YAP1 in CRC.

    Evidence Knockdown/overexpression, Western blotting of pathway nodes, Co-IP, and in vivo/specimen correlation across bladder, RCC, and CRC

    PMID:29702203 PMID:30037330 PMID:30158581

    Open questions at the time
    • Whether AKT/GSK3β effects depend on GAP catalysis not tested
    • Opposing YAP regulation across tissues unexplained
  7. 2019 Medium

    Identified IPO5-mediated nuclear translocation as a regulatory mechanism coupling RASAL2 localization to Ras activation in CRC, and uncovered exosome- and phosphorylation-based control of its tumor-suppressor/promoter balance in breast cancer.

    Evidence Mass spectrometry, Co-IP, subcellular fractionation for IPO5; CRISPR KO, exosome isolation, and phospho-Ser237 detection in breast cancer models

    PMID:31288861 PMID:31473883 PMID:31759919

    Open questions at the time
    • Functional role of nuclear RASAL2 beyond correlation with Ras activity unclear
    • How the p-Rasal2/non-p-Rasal2 ratio is set physiologically unknown
  8. 2021 High

    Defined the AMPKα-Ser351 phosphorylation switch governing RASAL2 control of autophagy, and showed GAP activity sustains basal Ras in TNBC via SPRY1/2 suppression with YAP as a transcriptional input.

    Evidence In vitro kinase assay, S351 mutagenesis, Co-IP with PPM1B and the VPS34 complex, PIK3C3 activity assay; ChIP for YAP-RASAL2 promoter and MEK/EGFR inhibitor synergy with GAP mutant

    PMID:33563064 PMID:34168046

    Open questions at the time
    • Upstream signals dictating Ser351 phosphorylation in tumors not defined
    • Whether the autophagy switch operates in the cancer contexts described elsewhere untested
  9. 2022 Medium

    Consolidated the oncogenic arm of RASAL2 across gastric, prostate, pancreatic, and hepatic contexts via AKT, β-catenin, cyclin D1, YAP1/TIAM1, and TET1/MTTP effectors, including NF-κB-driven induction and direct PP2A inhibition.

    Evidence ChIP, Co-IP (RASAL2-PP2A), PP2A activity assay, organoids, ubiquitination/hMeDIP assays, and in vivo models across gastric, prostate, PDAC, and liver

    PMID:35134322 PMID:35668070 PMID:35844783 PMID:36643045

    Open questions at the time
    • Why RASAL2 inhibits PP2A in some tissues yet suppresses AKT in others unresolved
    • Structural basis of PP2A binding undetermined
  10. 2023 Medium

    Identified CAMSAP2 as a regulator of RASAL2 stability, showing ubiquitin-proteasome degradation of RASAL2 unleashes ERK signaling to drive lung cancer metastasis.

    Evidence Co-IP, ubiquitin-proteasome assays, siRNA knockdown, and tail-vein metastasis model

    PMID:38159595

    Open questions at the time
    • The E3 ligase mediating degradation not identified
    • Whether CAMSAP2 acts as adaptor or scaffold unclear
  11. 2025 Medium

    Connected RASAL2 to secretory-autophagy exosome biology through direct inhibition of Rab27a in TNBC, and demonstrated a germline variant that hyperactivates Ras and confers anti-EGFR resistance.

    Evidence CRISPR KO, Co-IP (RASAL2-Rab27a), autophagosome/MVB colocalization, exosome characterization for Rab27a; functional p-ERK and cetuximab dose-response assays for the p.Y808C variant

    PMID:40369567 PMID:40849341

    Open questions at the time
    • Whether Rab27a inhibition is GAP-dependent untested
    • Clinical penetrance and disease association of p.Y808C not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • What determines whether RASAL2 functions as a GAP-dependent tumor suppressor or a GAP-independent oncogene in a given tissue remains the central unresolved question.
  • No unifying model integrating phosphorylation state, localization, and binding partners to predict suppressor vs. oncogene outcome
  • No high-resolution structure of RASAL2 or its complexes
  • Context-switch mechanism between PP2A/AKT activation and AKT/VEGFA suppression undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005634 nucleus 1 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-9612973 Autophagy 3 R-HSA-1643685 Disease 2

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 RASAL2 functions as a RasGAP tumor and metastasis suppressor in breast cancer; its ablation promotes Ras hyperactivation, tumor growth, progression, and metastasis in mouse models, establishing that RASAL2 loss is an alternative mechanism of activating Ras in cancer. Genetic ablation (knockout mouse models), in vivo tumor/metastasis assays, human breast cancer mutation/expression analysis Cancer cell High 24029233
2014 In triple-negative breast cancer (TNBC), RASAL2 acts independently of its RAS-GAP catalytic activity and instead promotes RAC1 signaling by binding and antagonizing the RAC1-GAP protein ARHGAP24, thereby driving mesenchymal invasion and metastasis. Co-immunoprecipitation (binding of RASAL2 to ARHGAP24), RAS-GAP catalytic mutant rescue experiments, RAC1 activity assays, shRNA knockdown/overexpression in TNBC cells The Journal of clinical investigation High 25384218
2014 RASAL2 knockdown in ovarian cancer cells activates the Ras-ERK pathway to promote EMT, migration, invasion, and tumor formation; pharmacological inhibition of the Ras-ERK pathway reverses the functional effects of RASAL2 depletion. shRNA knockdown, in vitro migration/invasion assays, in vivo tumor formation, ERK pathway inhibition rescue Oncotarget Medium 25216515
2012 RASAL2 physically interacts with ECT2 and regulates RHO GTPase activity in astrocytoma cells; RASAL2 knockdown causes conversion to an amoeboid migratory phenotype, identifying a role in mesenchymal-amoeboid transition. Cytoplasmic fractionation followed by ECT2 immunoprecipitation and mass spectrometry to identify RASAL2 as an ECT2-binding partner; RHO activity assay; RNA interference knockdown with phenotypic readout The American journal of pathology Medium 22683310
2017 RASAL2 suppresses bladder cancer stemness and EMT through the MAPK/SOX2 signaling axis; inhibition of ERK activity or knockdown of SOX2 reverses the stemness and mesenchymal properties induced by RASAL2 deficiency. Gain- and loss-of-function experiments in bladder cancer cells, ERK inhibitor and SOX2 siRNA rescue experiments, in vivo xenograft assays Cell death & disease Medium 28182001
2018 RASAL2 inhibits bladder cancer angiogenesis by suppressing AKT phosphorylation, which in turn reduces ETS1 expression and VEGFA levels; a negative correlation between RASAL2 and VEGFA/CD31 was confirmed in xenografts and human specimens. shRNA/siRNA knockdown and ectopic overexpression, Western blot for p-AKT/ETS1/VEGFA, in vivo xenograft and human specimen correlation Cellular signalling Medium 29702203
2018 RASAL2 knockdown in CRC cells promotes YAP1 phosphorylation, cytoplasmic retention, and ubiquitination, thereby activating the Hippo pathway through the LATS2/YAP1 axis; this oncogenic property was confirmed by co-immunoprecipitation. siRNA/shRNA knockdown, overexpression, expression microarray screening, co-immunoprecipitation, double immunofluorescence staining, in vivo studies Molecular cancer Medium 30037330
2018 RASAL2 activates GSK3β by reducing its Ser9 phosphorylation and subsequently decreases c-FOS and VEGFA expression to inhibit tumor angiogenesis in renal cell carcinoma. shRNA knockdown and overexpression, Western blot for p-GSK3β/c-FOS/VEGFA, specific inhibitor and siRNA rescue experiments, in vitro and in vivo angiogenesis assays Cell death & disease Medium 30158581
2019 IPO5 binds to the NLS sequence of RASAL2 to mediate its nuclear translocation; nuclear RASAL2 is associated with RAS signal activation, thereby promoting colorectal cancer progression. Mass spectrometry, co-immunoprecipitation, subcellular fractionation, immunofluorescence, in vivo and in vitro functional experiments Journal of experimental & clinical cancer research : CR Medium 31288861
2021 RASAL2 GAP activity suppresses negative feedback regulators SPRY1/2 and, together with EGFR upregulation, sustains basal RAS activity in TNBC; co-inhibition of MEK1/2 and EGFR induces synergistic apoptosis specifically in RASAL2-high tumors. YAP directly transcriptionally regulates RASAL2 expression. Transcriptional profiling, pharmacogenomic data mining, proteomic studies, in vitro and in vivo MEK/EGFR inhibitor combination treatment, GAP catalytic mutant experiments, chromatin immunoprecipitation (YAP-RASAL2 promoter) Clinical cancer research Medium 34168046
2021 PRKAA/AMPKα phosphorylates RASAL2 at Ser351 under glucose starvation; non-phosphorylated RASAL2 recruits phosphatase PPM1B to attenuate AMPKα phosphorylation and suppress basal autophagy, while phosphorylated RASAL2 binds the PIK3C3/VPS34-ATG14-BECN1 complex to increase PIK3C3 activity and promote autophagy, acting as a molecular switch. Co-immunoprecipitation (RASAL2 with PPM1B; phospho-RASAL2 with PIK3C3 complex), phosphorylation site mutagenesis (S351), double-knockout cells, PIK3C3 activity assay, autophagy flux assays Autophagy High 33563064
2019 Rasal2 knockout in MCF-7 breast cancer cells enhances exosomal release and increases autophagy-related proteins in the exosomal fraction; autophagy inhibition (3-MA) abrogates while autophagy blockade (chloroquine) facilitates Rasal2 KO-induced secretory autophagy-driven exosome release and consequent cancer cell proliferation. CRISPR-Cas9 knockout, exosome isolation and characterization, autophagy inhibitor treatments, cell proliferation assays Molecular and cellular biochemistry Medium 31473883
2019 Phosphorylation of Rasal2 at Serine 237 promotes tumor growth in both ER+ and ER- breast cancer cells; p-Rasal2 and non-p-Rasal2 exert their effects on cancer progression via exosome-mediated transport, with the p-Rasal2/non-p-Rasal2 ratio helping determine whether total Rasal2 acts as a tumor suppressor (ER+) or promoter (ER-). Western blot for phospho-Ser237-Rasal2, exosome purification and characterization by TEM and flow cytometry, in vivo and in vitro tumor growth experiments EBioMedicine Medium 31759919
2017 Rasal2 deficiency impairs adipogenesis in vitro and in vivo by increasing Ras and ERK activity in preadipocytes; Ras inhibition (but not ERK inhibition) rescues impaired adipogenesis, indicating that Rasal2 promotes adipogenesis by repressing Ras activity in an ERK-independent manner. Insertional mutant mice (Rasal2-deficient), 3T3-L1 preadipocyte siRNA knockdown, Ras/ERK activity assays, pharmacological rescue with Ras and MEK inhibitors Molecular metabolism Medium 28580280
2022 H. pylori infection induces RASAL2 expression via NF-κB directly binding the RASAL2 promoter; RASAL2 then inhibits protein phosphatase 2A (PP2A) activity through direct binding, leading to AKT activation and increased β-catenin transcriptional activity to drive gastric tumorigenesis. Chromatin immunoprecipitation (NF-κB at RASAL2 promoter), co-immunoprecipitation (RASAL2-PP2A), PP2A activity assay, gene silencing and ectopic overexpression, patient-derived organoids, in vivo xenograft models Gastroenterology High 35134322
2022 RASAL2 promotes prostate cancer cell proliferation and G1-to-S phase transition by facilitating AKT phosphorylation, which in turn increases cyclin D1 (CCND1) expression; a positive correlation between RASAL2 and cyclin D1 was confirmed in xenografts and clinical specimens. shRNA knockdown and overexpression, cell cycle analysis, Western blot for p-AKT/cyclin D1, in vivo xenograft studies, clinical specimen correlation Cell death discovery Medium 35668070
2022 RASAL2 deficiency attenuates hepatic steatosis by activating AKT signaling, which upregulates TET1 expression and promotes MTTP expression through DNA hydroxymethylation, increasing VLDL secretion from the liver. Chromatin immunoprecipitation assays, hydroxymethylated DNA immunoprecipitation (hMeDIP), in vivo VLDL secretion assay (tyloxapol injection), high-fat diet mouse model, in vitro hepatocyte model Journal of clinical and translational hepatology Medium 36643045
2022 RASAL2 promotes PDAC progression by accumulating TIAM1 expression: RASAL2 inhibits YAP1 phosphorylation (stabilizing YAP1), which increases TIAM1 mRNA expression and suppresses TIAM1 protein ubiquitination, thereby enhancing YAP1/TIAM1 signaling. shRNA knockdown and overexpression, Western blot for YAP1 phosphorylation/TIAM1, ubiquitination assays, in vitro and in vivo functional studies International journal of biological sciences Medium 35844783
2023 CAMSAP2 physically interacts with RASAL2 and facilitates its degradation through the ubiquitin-proteasome system, leading to ERK signaling activation and promotion of lung cancer metastasis. Proteomic/biochemical interaction analysis (BioGRID prediction followed by biochemical assays), Co-IP, ubiquitin-proteasome pathway assays, siRNA knockdown, in vivo tail vein metastasis model Life sciences Medium 38159595
2025 Rasal2 knockout in TNBC cells disrupts autophagic flux and induces secretory autophagy; Rasal2 directly binds Rab27a (confirmed by Co-IP) and inhibits its activity, and Rab27a knockdown suppresses Rasal2 KO-induced autophagic-exosome secretion and TNBC progression. CRISPR-Cas9 knockout, siRNA knockdown, Co-immunoprecipitation (RASAL2-Rab27a), confocal microscopy of autophagosome/MVB colocalization, NTA/TEM for exosome characterization, in vivo xenograft Journal of translational medicine Medium 40369567
2025 The germline RASAL2 c.2423 A>G variant (p.Y808C) enhances RAS signaling with sustained ERK phosphorylation and increases CRC cell proliferation; mutant cells require higher doses of cetuximab for ERK suppression, conferring resistance to anti-EGFR therapy via abnormal RAS activation. Functional cell-based assays (ERK phosphorylation, proliferation), cetuximab dose-response experiments, population frequency analysis Scientific reports Medium 40849341

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 The RasGAP gene, RASAL2, is a tumor and metastasis suppressor. Cancer cell 113 24029233
2014 RASAL2 activates RAC1 to promote triple-negative breast cancer progression. The Journal of clinical investigation 81 25384218
2016 miR-136 suppresses tumor invasion and metastasis by targeting RASAL2 in triple-negative breast cancer. Oncology reports 75 27108696
2022 Helicobacter pylori-induced RASAL2 Through Activation of Nuclear Factor-κB Promotes Gastric Tumorigenesis via β-catenin Signaling Axis. Gastroenterology 71 35134322
2018 RASAL2 promotes tumor progression through LATS2/YAP1 axis of hippo signaling pathway in colorectal cancer. Molecular cancer 63 30037330
2014 RASAL2 down-regulation in ovarian cancer promotes epithelial-mesenchymal transition and metastasis. Oncotarget 49 25216515
2017 RASAL2, a RAS GTPase-activating protein, inhibits stemness and epithelial-mesenchymal transition via MAPK/SOX2 pathway in bladder cancer. Cell death & disease 40 28182001
2012 ECT2 and RASAL2 mediate mesenchymal-amoeboid transition in human astrocytoma cells. The American journal of pathology 37 22683310
2019 Sulforaphane Induces miR135b-5p and Its Target Gene, RASAL2, thereby Inhibiting the Progression of Pancreatic Cancer. Molecular therapy oncolytics 36 31044154
2019 IPO5 promotes the proliferation and tumourigenicity of colorectal cancer cells by mediating RASAL2 nuclear transportation. Journal of experimental & clinical cancer research : CR 36 31288861
2014 RASAL2 promotes lung cancer metastasis through epithelial-mesenchymal transition. Biochemical and biophysical research communications 30 25446096
2018 The expression and function of RASAL2 in renal cell carcinoma angiogenesis. Cell death & disease 23 30158581
2020 miR‑654‑3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non‑small‑cell lung cancer. Molecular medicine reports 21 33300072
2018 RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer. Cellular signalling 20 29702203
2017 Upregulation of RASAL2 promotes proliferation and metastasis, and is targeted by miR-203 in hepatocellular carcinoma. Molecular medicine reports 20 28447723
2021 RASAL2 Confers Collateral MEK/EGFR Dependency in Chemoresistant Triple-Negative Breast Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 19 34168046
2019 Rasal2 suppresses breast cancer cell proliferation modulated by secretory autophagy. Molecular and cellular biochemistry 19 31473883
2019 RASAL2 Plays Inconsistent Roles in Different Cancers. Frontiers in oncology 19 31799194
2017 Downregulation of RASAL2 promotes the proliferation, epithelial-mesenchymal transition and metastasis of colorectal cancer cells. Oncology letters 19 28454265
2021 PRKAA/AMPKα phosphorylation switches the role of RASAL2 from a suppressor to an activator of autophagy. Autophagy 18 33563064
2015 RASAL2 inhibited the proliferation and metastasis capability of nasopharyngeal carcinoma. International journal of clinical and experimental medicine 16 26770493
2017 Rasal2 deficiency reduces adipogenesis and occurrence of obesity-related disorders. Molecular metabolism 14 28580280
2022 RASAL2 regulates the cell cycle and cyclin D1 expression through PI3K/AKT signalling in prostate tumorigenesis. Cell death discovery 13 35668070
2019 Phosphorylated Rasal2 facilitates breast cancer progression. EBioMedicine 13 31759919
2020 MicroRNA-876-5p represses the cell proliferation and invasion of colorectal cancer through suppressing YAP signalling via targeting RASAL2. Clinical and experimental pharmacology & physiology 11 31990059
2013 RASAL2: wrestling in the combat of Ras activation. Cancer cell 9 24029223
2024 LncRNA RASAL2-AS1 promotes METTL14-mediated m6A methylation in the proliferation and progression of head and neck squamous cell carcinoma. Cancer cell international 8 38528591
2022 RASAL2 Deficiency Attenuates Hepatic Steatosis by Promoting Hepatic VLDL Secretion via the AKT/TET1/MTTP Axis. Journal of clinical and translational hepatology 7 36643045
2021 Low Expression of Rasal2 Promotes Non-small Cell Lung Cancer Metastasis through Ras/ERK Pathway. Biological & pharmaceutical bulletin 7 34193694
2020 Suppressive effects of RASAL2 on renal cell carcinoma via SOX2/ERK/p38 MAPK pathway. Experimental and therapeutic medicine 6 33093889
2024 RAS protein activator-like 2 (RASAL2) initiates peritubular capillary rarefaction in hypoxic renal interstitial fibrosis. Translational research : the journal of laboratory and clinical medicine 5 38453052
2023 Germline variation in RASAL2 may predict survival in patients with RAS-activated colorectal cancer. Genes, chromosomes & cancer 5 36790221
2023 CAMSAP2 enhances lung cancer cell metastasis by mediating RASAL2 degradation. Life sciences 5 38159595
2025 Rasal2 inhibits autophagic-exosomes secretion via regulating Rab27a in triple-negative breast cancer progression. Journal of translational medicine 3 40369567
2022 RASAL2 mediated the enhancement of YAP1/TIAM1 signaling promotes malignant phenotypes of pancreatic ductal adenocarcinoma. International journal of biological sciences 3 35844783
2021 RASAL2 suppresses the proliferative and invasive ability of PC3 prostate cancer cells. Oncotarget 3 34966481
2015 [Expression of RASAL2 in hepatocellular carcinoma and the clinical significance]. Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences 2 25832527
2026 A novel role of follicular fluid exosomal miR-143-5p in polycystic ovary syndrome: targeting RASAL2 to drive granulosa cell proliferation. Molecular and cellular endocrinology 0 42208847
2025 The RASAL2 variant promotes aberrant RAS signaling and resistance to anti-EGFR therapy in colorectal cancer. Scientific reports 0 40849341

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