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CD2-binding protein 2 (CD2BP2)

Target
CD2BP2
Molecular classification
Splicing factor, Adaptor protein, Other (RNA-binding protein, not a receptor, enzyme, transporter, or classical druggable target)
01

Overview

CD2-binding protein 2 is an adaptor protein and essential component of the spliceosome, particularly the U5 small nuclear ribonucleoprotein (snRNP) complex, involved in the precise excision of introns from pre-mRNA. It contains a conserved GYF domain mediating specific protein-protein interactions[1][3]. While originally identified as a binding partner of the CD2 T-cell surface antigen (implicating a minor role in T cell signaling), its critical cellular function is in the nucleus, enabling accurate mRNA splicing and microRNA stability. Loss of CD2BP2 impairs T cell development through altered splicing of transcripts controlling proliferation and apoptosis[3]. Alternative and divergent transcript variants are predicted but not characterized for biological activity or therapeutic relevance[1]. "CD2BP2 divergent transcript" (CD2BP2-DT) likely refers to an uncharacterized alternative transcript, not an established protein or therapeutic target. For structured data, use the well-characterized “CD2-binding protein 2 (CD2BP2)” as the canonical entry. Alternative transcripts remain to be experimentally validated for function[1][3].

Other names
SNU40U5-52KLIN1FWP010PPP1R59
02

Mechanism of action

Not applicable.

03

Biological functions

Pre-mRNA splicing (component of U5 snRNP within the spliceosome)Regulation of T lymphocyte activation (binds the cytoplasmic tail of CD2, but primary importance is in splicing, not surface signaling)Post-transcriptional gene regulation via microRNA complexes
04

Disease associations

Immune system development (especially T cell maturation and homeostasis through splicing regulation)Potential links to cancer and apoptosis via RNA splicing fidelity, but not a direct cancer geneOther (general role in RNA biology; not directly cited in main disease categories as a therapeutic target)
05

Safety considerations

None specifically known, since this is not a direct therapeutic target. However, as a core mRNA splicing factor, broad inhibition would compromise cellular viability and lead to global transcriptome dysregulation.

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