Seroatlas · Human Serome Atlas

TAGLN2

Transgelin-2

Also known as: HA1756, KIAA0120, TAGL2_HUMAN

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession: P37802
Gene: TAGLN2
Ensembl: ENSG00000158710
Chromosome: 1
Canonical length: 199 aa
Protein class: Plasma proteins, Predicted intracellular proteins
Subcellular location: Vesicles,Actin filaments,Basal body,Cytosol

OverviewNCBI Gene

The protein encoded by this gene is similar to the protein transgelin, which is one of the earliest markers of differentiated smooth muscle. The specific function of this protein has not yet been determined, although it is thought to be a tumor suppressor. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Mar 2013]

Canonical amino-acid sequenceUniProt

199 residues, UniProt reviewed canonical sequence.

>P37802|TAGLN2
     1  MANRGPAYGL SREVQQKIEK QYDADLEQIL IQWITTQCRK DVGRPQPGRE NFQNWLKDGT
    61  VLCELINALY PEGQAPVKKI QASTMAFKQM EQISQFLQAA ERYGINTTDI FQTVDLWEGK
   121  NMACVQRTLM NLGGLAVARD DGLFSGDPNW FPKKSKENPR NFSDNQLQEG KNVIGLQMGT
   181  NRGASQAGMT GYGMPRQIL

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against TAGLN2 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.

Antibody reachability: Secreted
Secreted: Yes
Transmembrane segments: 0
Mean surface accessibility (rSASA): 0.38
Highest tissue expression: 783 nTPM

Expression across tissuesHPA

Tissue

lung: 783 nTPM
stomach: 659 nTPM
esophagus: 568 nTPM
spleen: 548 nTPM
skin: 478 nTPM
blood vessel: 459 nTPM

Single-cell type

platelets: 5,154 nCPM
extravillous trophoblasts: 3,048 nCPM
megakaryocytes: 2,331 nCPM
migrating cytotrophoblasts: 900 nCPM
neutrophils: 886 nCPM
foveolar cells: 878 nCPM

Immune cell

neutrophil: 3,764 nTPM
eosinophil: 3,170 nTPM
total PBMC: 2,258 nTPM
plasmacytoid DC: 1,971 nTPM
basophil: 1,462 nTPM
myeloid DC: 1,180 nTPM

Brain region

hypothalamus: 172 nTPM
medulla oblongata: 147 nTPM
spinal cord: 113 nTPM
thalamus: 107 nTPM
pons: 99 nTPM
midbrain: 97 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about TAGLN2.

Disease | ImmuneIEDB

Conditions an epitope on TAGLN2 was assayed in.

rheumatoid arthritis B cell
type 1 diabetes mellitus T cell

Genetic constraint and essentialitygnomAD · DepMap

Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.

gnomAD LOEUF (loss-of-function intolerance): 0.93
gnomAD pLI: 0.01
gnomAD missense Z: 0.71
DepMap mean gene effect: -0.16
DepMap dependency class: selective

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 9% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of TAGLN2 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.

TAGLN3

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads TAGLN2 as an antibody target. Whether an autoantibody or antibody against TAGLN2 could matter depends on whether native TAGLN2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

TAGLN2 is annotated as secreted, so native TAGLN2 circulates and is directly accessible to antibodies. Secreted and cell-surface proteins are the autoantibody targets most likely to act like drugs, blocking or depleting the native protein.

Annotation status

The present source text does not explicitly label TAGLN2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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