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FLASH GENE
Symbol PLS3 contributors: mct/npt - updated : 25-04-2023
HGNC name plastin 3 (T isoform)
HGNC id 9091
EXPRESSION
Type ubiquitous
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Digestiveesophagus   highly
Lymphoid/Immunespleen   highly
Nervousspinal cord   highly
Respiratorydiaphragm   highly Homo sapiensFetal
 lung   highly Homo sapiens
Urinarykidney   highly
cell lineage
cell lines
fluid/secretion
at STAGE
physiological period fetal
Text highly expressed in the fetal spinal cord
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • N-terminal calcium-binding region and
  • two C-terminal actin-binding domains, which are each composed of two calponin homology domains
  • HOMOLOGY
    Homologene
    FAMILY
    CATEGORY transcription factor
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm,cytosolic
    text
  • PLS3 and CORO1C are strongly enriched in lamellipodia structures at growing edges under the plasma membrane
  • basic FUNCTION
  • playing an important role for axonogenesis through increasing the F-actin level
  • playing a role during neuronal differentiation
  • PLS3 gene may have an age- and gender-specific role in the clinical severity of SMA in children afflicted with this condition
  • is an actin-binding/bundling protein, with a role in Ca(2+) regulation that is essential for the function of PLS3 in motor axons
  • is a protein involved in actin bundle formation in the cytoskeleton
  • is a genuine SMA protective modifier
  • PLS3 is a modifier of SMA in motor-neurons (MN)
  • F-actin binding and bundling protein
  • in SMA, PLS3 and CORO1C but not TMOD3 play an important role in endocytosis by restoring F-actin-dependent processes
  • influences bone homeostasis through regulation of osteoclast activity
  • PLS3 serves an important role in EMT
  • plays a key role in cancer cell proliferation and invasion
  • Ca2+-dependent F-actin binding and bundling protein, associated with pathologies of the musculoskeletal system, nephrological disorders, malignancies of the solid and hematopoietic system, and numerous neuromuscular disorders
  • PLS3 is able to escape X chromosome inactivation in spinal MN
  • in contrast to the DXZ4 copy number, the regulation of PLS3 by CHD4/NuRD is not sex-specific
  • is regulated in a tissue-specific manner during embryonic development
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • two actin-related binding partners of PLS3, are CORO1C, and TMOD3
  • NCALD acts as a negative regulator of endocytosis, which is in contrast to PLS3 acting as its positive regulator
  • NKRF is a novel PLS3 interactor, which increasingly translocates to the nucleus when PLS3 is overexpressed
  • CHD4 is a transcriptional regulator of PLS3, and interaction positively regulates the expression of PLS3
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s) MRDO , COPO , DIH5
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    rescued the axon length and outgrowth defects associated with SMN down-regulation in motor neurons
    constitutional     --over  
    in actively dividing cells and up-regulated in several carcinomas
    constitutional     --over  
    hypomethylation is associated with overexpression of PLS3, GATA6, and TWIST1 in the Sezary Syndrome
    constitutional     --low  
    contributes to SMA motor phenotypes
    tumoral     --over  
    has significantly poorer prognosis than the low expression in gastric cancer
    Susceptibility
    Variant & Polymorphism
    Candidate gene useful molecular marker for predicting the responsiveness of cancer cells to treatment with chemotherapeutic drugs
    Marker
  • PLS3 is a biomarker to estimate pancreatic cancer progression for pancreatic cancer therapy
  • high PLS3 expression was an independent prognostic factor for survival in gastric cancer
  • Therapy target
    SystemTypeDisorderPubmed
    neuromuscularspinal muscular atrophy 
    power of PLS3 and CORO1C modidfiers to unravel the cellular pathomechanisms underlying SMA and the power of combinatorial therapy based on splice correction of SMN2 and endocytosis improvement to efficiently treat SMA
    cancerdigestivepancreas
    molecular target for pancreatic cancer therapy
    ANIMAL & CELL MODELS
  • endocytosis is disturbed in the NMJ of SMA mice and this disturbance is counteracted by Pls3 overexpression