Protein / target

Tyrosine-protein phosphatase non-receptor type 11

Encoded byPTPN11Q06124Homo sapiensSwiss-Prot

UniProt: Q06124 Ensembl: ENSG00000179295 HGNC: HGNC:9644 NCBI Gene: 5781

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

Advanced Clinical

Research papers

Protein at a glance

Biological role

Non-membrane spanning protein tyrosine phosphatase

Strongest disease association

RASopathy

Via encoding gene PTPN11 · Genetic evidence · score 0.97

Therapeutic position

Clinically advancing target

Small molecules

Research activity

Emerging research

1 papers · latest 2023

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Acts downstream of various receptor and cytoplasmic protein tyrosine kinases to participate in the signal transduction from the cell surface to the nucleus.

View complete UniProt function annotation

Acts downstream of various receptor and cytoplasmic protein tyrosine kinases to participate in the signal transduction from the cell surface to the nucleus (PubMed:10655584, PubMed:14739280, PubMed:18559669, PubMed:18829466, PubMed:26742426, PubMed:28074573, PubMed:32184441). Positively regulates MAPK signal transduction pathway (PubMed:28074573). Dephosphorylates GAB1, ARHGAP35 and EGFR (PubMed:28074573). Dephosphorylates ROCK2 at 'Tyr-722' resulting in stimulation of its RhoA binding activity (PubMed:18559669). Dephosphorylates CDC73 (PubMed:26742426). Dephosphorylates SOX9 on tyrosine residues, leading to inactivate SOX9 and promote ossification (By similarity). Dephosphorylates tyrosine-phosphorylated NEDD9/CAS-L (PubMed:19275884). Acts as an effector of PDCD1-mediated inhibition of T-cell response: recruited by phosphorylated PDCD1, mediating dephosphorylation of key T-cell receptor (TCR) proximal signaling molecules, leading to TCR signaling inhibition (PubMed:32184441)

Subcellular location

CytoplasmNucleus

Domains and Gene Ontology detail (58)

Domains & features

SH2 1SH2 2Tyrosine-protein phosphatase

Gene Ontology

Ccytoplasm
Ccytosol
Cfocal adhesion
Cmitochondrion
Cnucleolus
Cnucleoplasm
Cnucleus
Cprotein-containing complex
Fcadherin binding
Fcell adhesion molecule binding
Finsulin receptor binding
Fmolecular adaptor activity

593 aa · 68 kDa · 3 isoforms

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Growth-factor signallingGOReceptor tyrosine kinase signallingGOImmune signallingGOCell adhesionGO

View supporting evidence

Growth-factor signalling

·cellular response to epidermal growth factor stimulus
·epidermal growth factor receptor signaling pathway
·fibroblast growth factor receptor signaling pathway

Receptor tyrosine kinase signalling

·receptor tyrosine kinase binding
·ERBB signaling pathway

Immune signalling

·cytokine-mediated signaling pathway
·negative regulation of T cell activation
·negative regulation of T cell proliferation
·negative regulation of T cell receptor signaling pathway

Cell adhesion

·cell adhesion molecule binding
·negative regulation of cell adhesion mediated by integrin

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene PTPN11

Gene-level evidence surfaced through the gene PTPN11that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Noonan syndrome

0.98Well supported

Genetic evidence dominant · Open Targets 0.88

RASopathy

0.97Well supported

Genetic evidence dominant · Open Targets 0.59

Noonan syndrome with multiple lentigines

0.93Well supported

Genetic evidence dominant · Open Targets 0.84

Leukemia, Myeloid, Acute

0.65Moderately supported

Somatic mutation evidence dominant · Open Targets 0.64

Neoplasms

0.56Moderately supported

Pathway evidence dominant · Open Targets 0.61

View evidence synthesis (5)

Noonan syndromeWell supported

0.98

agreement 0.88–1.00

Genetic60%Somatic mutation22%Animal model14%Literature3%Genetic literaturedup

Open Targets aggregate 0.88 · 4 independent evidence families · 1 not counted as duplicate

RASopathyWell supported

0.97

agreement 0.83–1.00

Genetic96%Literature4%

Open Targets aggregate 0.59 · 2 independent evidence families

Noonan syndrome with multiple lentiginesWell supported

0.93

agreement 0.81–1.00

Genetic78%Animal model18%Literature4%Genetic literaturedup

Open Targets aggregate 0.84 · 3 independent evidence families · 1 not counted as duplicate

Leukemia, Myeloid, AcuteModerately supported

0.65

agreement 0.52–0.79

Somatic mutation64%Pathway19%Literature17%

Open Targets aggregate 0.64 · 3 independent evidence families

NeoplasmsModerately supported

0.56

agreement 0.44–0.68

Pathway53%Genetic26%Literature20%

Open Targets aggregate 0.61 · 3 independent evidence families

The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations

Noonan syndrome0.88

Noonan syndrome with multiple lentigines0.84

Leukemia, Myeloid, Acute0.64

Neoplasms0.61

RASopathy0.59

Drug development

1 compounds recorded · 1 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (1)

BATOPROTAFIBPhase 1 2

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Small molecules — Strong

Advanced Clinical and Structure with Ligand support this modality.

Protein degraders — Emerging

Feasibility evidence (literature and database ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (8)

SM · Advanced ClinicalSM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyPR · LiteraturePR · Database UbiquitinationPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

regulation of catalytic activityToxCast

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.

Research activity

1 papers · to 2023

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

SHP2: A Pleiotropic Target at the Interface of Cancer and Its Microenvironment.69 cites

Sodir NM · Cancer discovery · 2023

Recent

SHP2: A Pleiotropic Target at the Interface of Cancer and Its Microenvironment.

Sodir NM · Cancer discovery · 2023

Europe PMC papers linked directly to this protein.