gene

CBL

Entity Detail — Knowledge Graph Node

Understanding Entity Pages

This page aggregates everything SciDEX knows about CBL: its mechanistic relationships (Knowledge Graph edges), hypotheses targeting it, analyses mentioning it, and supporting scientific papers. The interactive graph below shows its immediate neighbors. All content is AI-synthesized from peer-reviewed literature.

158Connections

0Hypotheses

0Analyses

50Outgoing

25Incoming

0Experiments

0Debates

Summary

CBL is a gene implicated in neurodegeneration research. Key relationships include: activates, interacts with, associated with. Associated with Aging, Als, Alzheimer. Connected to 83 entities in the SciDEX knowledge graph.

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🧬 Gene Info

Gene Symbol	CBL
Full Name	Casitas B-lineage Lymphoma
Chromosome	11q23.3
Protein Type	Ligase
Function	encodes a RING-type E3 ubiquitin ligase that serves as a critical negative regulator of receptor tyrosine kinase (RTK) signaling.
Molecular Weight	100 kDa
Amino Acids	906 aa
Pathways	Inflammasome
UniProt ID	[P22681](https://www.uniprot.org/uniprot/P22681)
Ensembl ID	ENSG00000110395
GeneCards	CBL
Human Protein Atlas	CBL
Linker Region	Connects TKB and RING domains, regulatory function
C-terminal Proline-Rich Region	Mediates protein-protein interactions with SH3 domain-containing proteins
UEV Domain	Ubiquitin-conjugating enzyme variant, substrate recognition
Associated Diseases	Als, Alzheimer, Infection, Inflammation, Lymphoma
Interactions	ACVR1, AKT, AND, APOPTOSIS, ASC, BAX
KG Connections	158 knowledge graph edges
Databases	GeneCards NCBI Gene HPA STRING

Wiki Pages (4)

Knowledge base pages for this entity

Canonical Page

Pathway Diagram

graph TD
    CBL["CBL"]
    Traumatic_Brain_Injury{"Traumatic Brain Injury"}
    CBL -->|"therapeutic target"| Traumatic_Brain_Injury
    Als{"Als"}
    CBL -->|"therapeutic target"| Als
    CBL -->|"regulates"| Als
    Ms{"Ms"}
    CBL -->|"regulates"| Ms
    Aging{"Aging"}
    CBL -->|"interacts with"| Aging
    CBL -->|"interacts with"| Als
    Cancer{"Cancer"}
    CBL -->|"interacts with"| Cancer
    Lymphoma{"Lymphoma"}
    CBL -->|"associated with"| Lymphoma
    Tumor{"Tumor"}
    CBL -->|"interacts with"| Tumor
    FOXO4["FOXO4"]
    CBL -->|"activates"| FOXO4
    PDGFRB["PDGFRB"]
    CBL -->|"associated with"| PDGFRB
    HSP90AB1["HSP90AB1"]
    CBL -->|"associated with"| HSP90AB1
    NDUFA2["NDUFA2"]
    NDUFA2 -->|"associated with"| CBL
    NDUFS6["NDUFS6"]
    NDUFS6 -->|"associated with"| CBL
    NDUFA1["NDUFA1"]
    NDUFA1 -->|"associated with"| CBL
    PIK3CA["PIK3CA"]
    PIK3CA -->|"associated with"| CBL
    RANKINGS["RANKINGS"]
    RANKINGS -->|"associated with"| CBL
    RAC1["RAC1"]
    RAC1 -->|"interacts with"| CBL
    MAPK1["MAPK1"]
    MAPK1 -->|"associated with"| CBL
    PI3K["PI3K"]
    PI3K -->|"interacts with"| CBL
    style CBL fill:#1a3a4a,stroke:#4fc3f7,stroke-width:3px,color:#e0e0e0

Outgoing (133)

Target	Relation	Type	Str
HNRNPA2B1	degrades	protein	0.92
Hnrnpa2B1	degrades	protein	0.88
Inflammation	activates	disease	0.75
Als	activates	disease	0.75
Mapk	associated_with	pathway	0.70
Traumatic Brain Injury	therapeutic_target	disease	0.65
Als	causes	disease	0.65
Als	associated_with	disease	0.65
Traumatic Brain Injury	inhibits	disease	0.65
Inflammation	inhibits	disease	0.65
Neurodegeneration	causes	disease	0.65
Neuroinflammation	inhibits	disease	0.65
Ms	associated_with	disease	0.65
Als	therapeutic_target	disease	0.65
Alzheimer	causes	disease	0.65
Lymphoma	associated_with	disease	0.65
Cancer	interacts_with	disease	0.65
Tumor	interacts_with	disease	0.65
Infection	causes	disease	0.65
Insulin Resistance	activates	disease	0.65
ALS	inhibits	disease	0.65
Tumor	activates	disease	0.65
Als	regulates	disease	0.65
Metabolic Syndrome	activates	disease	0.65
Ms	regulates	disease	0.65
Als	inhibits	disease	0.65
Lymphoma	regulates	disease	0.65
Melanoma	inhibits	disease	0.65
Als	interacts_with	disease	0.65
Aging	interacts_with	disease	0.65
Inflammation	causes	disease	0.65
Immune Response	activates	pathway	0.60
Innate Immunity	activates	pathway	0.60
INFLAMMATION	causes	gene	0.60
Apoptosis	activates	pathway	0.60
ALZHEIMER	causes	gene	0.60
INFLAMMATION	activates	gene	0.60
NF-ΚB	activates	gene	0.60
NEURODEGENERATION	causes	gene	0.60
APOPTOSIS	activates	gene	0.60
ERK	causes	gene	0.60
Insulin Signaling	activates	pathway	0.60
RAS	activates	gene	0.60
APOPTOSIS	inhibits	gene	0.60
AND	inhibits	gene	0.60
Neuron	inhibits	cell_type	0.60
Apoptosis	inhibits	pathway	0.60
Synaptic Plasticity	associated_with	pathway	0.60
MICROGLIA	associated_with	gene	0.60
RAS	associated_with	gene	0.60

Incoming (25)

Source	Relation	Type	Str
genes-cbl	linked_to	wiki_page	1.00
LNK	interacts_with	protein	0.95
NDUFS6	associated_with	gene	0.60
NDUFA1	associated_with	gene	0.60
NRAS	associated_with	gene	0.60
BRAF	associated_with	gene	0.60
NDUFA2	associated_with	gene	0.60
TLR4	inhibits	gene	0.60
TLR2	inhibits	gene	0.60
TNF	inhibits	gene	0.60
RAF1	associated_with	gene	0.60
PIK3CA	associated_with	gene	0.60
RANKINGS	associated_with	gene	0.60
RAC1	interacts_with	gene	0.60
MAPK1	associated_with	gene	0.60
PI3K	interacts_with	gene	0.60
MAPK	associated_with	gene	0.60
KRAS	associated_with	gene	0.60
BAX	inhibits	gene	0.60
TLR	inhibits	gene	0.60
ROS	inhibits	gene	0.60
APOPTOSIS	inhibits	gene	0.60
NEUROINFLAMMATION	inhibits	gene	0.60
CYTOKINES	activates	gene	0.60
BRAIN INJURY	inhibits	gene	0.60

Targeting Hypotheses (0)

Hypotheses where this entity is a therapeutic target

Hypothesis	Score	Disease	Analysis
No targeting hypotheses

Mentioning Analyses (0)

Scientific analyses that reference this entity

No analyses mention this entity

Experiments (0)

Experimental studies targeting or related to this entity

Experiment	Type	Disease	Score	Feasibility	Model	Status	Est. Cost
No experiments found

Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMID	Authors	Journal	Year	Citations
No papers found

Debates (0)

Multi-agent debates referencing this entity

No debates reference this entity

Related Research

Hypotheses and analyses mentioning CBL in their description or question text

No additional research found

CBL