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FLASH GENE
Symbol LMO7 contributors: mct - updated : 08-01-2020
HGNC name LIM domain only 7
HGNC id 6646
EXPRESSION
Type
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
blood / hematopoieticthymus   lowly
Cardiovascularheart   highly
Digestiveintestinelarge intestinecolon lowly
 liver   lowly
Endocrineadrenal gland   lowly
 pancreas    
Hearing/Equilibriumearinner  lowly Homo sapiens
Nervousbrain    
Reproductivemale systemtestis  lowly
 male systemprostate  lowly
Respiratorylung   highly Homo sapiens
Urinarykidney   highly
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Epithelial    
Muscularstriatumskeletal  
Nervouscentral   
cells
SystemCellPubmedSpeciesStageRna symbol
Blood/Hematopoieticleukocyte
cell lineage
cell lines
fluid/secretion
at STAGE
physiological period fetal
Text lung,heart
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a calponin homology (CH) domain, a one PDZ domain, a C terminal LIM domain
  • an F-Box (FBX) domain is present in alternative splice variants
  • HOMOLOGY
    Homologene
    FAMILY LMO gene family
    CATEGORY regulatory , transcription factor
    SUBCELLULAR LOCALIZATION     plasma membrane,junction
        intracellular
    intracellular,cytoplasm,cytosolic
    intracellular,nucleus
    text
  • specifically localized in the cuticular plate and the cell junction
  • basic FUNCTION
  • regulating emerin gene expression
  • forming a specific protein-binding interface for protein-protein interactions
  • MLLT4- and ACTN1-binding protein that connects the PVRL1-MLLT4 and E-cadherin-catenin systems through alpha-actinin
  • regulating development
  • possible essential functions for LMO7 during vertebrate heart development
  • required for proper myoblast differentiation
  • cell-specific regulator of myocardin-related transcription factors (MRTFs) and plays an important role in breast cancer cell migration
  • colocalizes with F-actin and reduces the G-actin/F-actin ratio via a Rho-independent mechanism
  • LMO7 is dispensable for skeletal muscle and cardiac physiology and pathophysiology
  • LMO7 via its LIM domain acts to control mitosis progression and exerts an effect on the SAC
  • LMO7 is induced by TGFB1 and serves to limit vascular fibrotic responses through negative feedback regulation of the TGFB1 pathway
  • CELLULAR PROCESS nucleotide, transcription
    PHYSIOLOGICAL PROCESS development
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule metal binding,
    zinc Zn2+
    protein
  • binding emerin protein, and EDMD-relevant genes
  • required for emerin gene transcription
  • feedback-regulated by binding to emerin
  • bound alpha-actinin, an actin filament-bundling protein, which bound to alpha-catenin
  • EMD binds to and inhibits the activity of LMO7, a transcription factor that regulates the expression of genes implicated in EMD (functional interaction between emerin and LMO7 is crucial for temporally regulating the expression of key myogenic differentiation genes)
  • interacted with the spindle assembly checkpoint (SAC) protein MAD1L1
  • LMO7 and LIMCH1 were identified as interaction partners to LRIG3
  • LMO7 and LIMCH1 physically interact with LRIG proteins
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    in the stroma of invasive breast carcinoma in a manner that correlates with the increased expression of SRF target genes that regulate muscle and actin cytoskeleton functions
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • deletion of Uchl3 and Lmo7 on mouse chromosome 14 causes defects in viability, postnatal growth and degeneration of muscle and retina
  • Lmo7-null mice had growth retardation, decreased fiber size, and impaired skeletal muscle and cardiac function, and loss of Lmo7 in mice causes myopathic phenotypes similar to those seen in other EDMD mouse models