Cell Adhesion Molecules of the Immunoglobulin Superfamily in the Nervous System

Walmod, Peter S.; Pedersen, Maria; Berezin, Vladimir; Bock, Elisabeth

doi:10.1007/978-0-387-30379-6_2

Cited by 17 publications

(17 citation statements)

References 781 publications

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“…Furthermore, BASP1 could not substitute for GAP‐43 as a downstream target in NCAM‐mediated neurite outgrowth. These results demonstrate that BASP1 induces neurite outgrowth in part by modulating signal transduction pathways entirely different from those activated during neurite outgrowth induced by NCAM and several other cell adhesion molecules (Walmod et al, 2007). However, the stimulatory effects of BASP1 on neurite outgrowth were completely inhibited when the membrane localization of the protein was abrogated, suggesting that the membrane localization and/or modulation of membrane structure is of pivotal importance for the neurite‐promoting function of the protein.…”

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confidence: 66%

“…In the nervous system, NCAM‐180 is expressed only by neurons, NCAM‐140 is expressed by neurons and glial cells, whereas NCAM‐120 is expressed only by glial cells. The extracellular part of NCAM is involved in both homophilic and heterophilic interactions (Walmod et al, 2007), and the protein can induce neurite outgrowth through the activation of several intracellular signal transduction pathways, including signaling via Fyn‐FAK (Beggs et al, 1997) and the fibroblast growth factor receptor (FGFR; Doherty and Walsh, 1996; Hinsby et al, 2004).…”

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confidence: 99%

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Characterization of BASP1‐mediated neurite outgrowth

Korshunova

Caroni²,

Kolkova

et al. 2008

J of Neuroscience Research

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The brain acid-soluble protein BASP1 (CAP-23, NAP-22) belongs to the family of growth-associated proteins, which also includes GAP-43, a protein recently shown to regulate neural cell adhesion molecule (NCAM)-mediated neurite outgrowth. Here, the effects of BASP1 overexpression were investigated in PC12E2 cells and primary hippocampal neurons. BASP1 overexpression stimulated neurite outgrowth in both cell types. The effects of BASP1 and trans-homophilic NCAM interactions were additive, and BASP1-induced neurite outgrowth was not inhibited by ectopic expression of cytoplasmic NCAM domains. Furthermore, inhibition of signaling via the fibroblast growth factor receptor, Src-family nonreceptor tyrosine kinases, protein kinase C, or GSK3beta, and expression of constructs of the cytoskeletal proteins spectrin and tau inhibited NCAM- but not BASP1-induced neurite outgrowth. Expression of BASP1 mutated at the serine-5 phosphorylation site stimulated neurite outgrowth to a degree comparable to that observed in response to overexpression of wild-type BASP1, whereas expression of BASP1 mutated at the myristoylation site at glycine-1 completely abrogated the stimulatory effects of the protein on neurite outgrowth. Finally, coexpression experiments with dominant negative and wild-type versions of GAP-43 and BASP1 demonstrated that the two proteins could substitute for each other with respect to induction of NCAM-independent neurite outgrowth, whereas BASP1 was unable to replace the stimulatory effect of GAP-43 on NCAM-mediated neurite outgrowth. These observations demonstrate that BASP1 and GAP-43 have overlapping, but not identical, functions in relation to neurite outgrowth and indicate that the main function of BASP1 is to regulate the organization and morphology of the plasma membrane.

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confidence: 66%

mentioning

confidence: 99%

Characterization of BASP1‐mediated neurite outgrowth

Korshunova

Caroni²,

Kolkova

et al. 2008

J of Neuroscience Research

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“…Neural cell adhesion molecule is well known for its ability to promote neurite outgrowth (see Walmod et al. 2007).…”

Section: Resultsmentioning

confidence: 99%

“…In addition to its effects on neurite outgrowth, NCAM is known to be involved in neuroprotection (see Walmod et al. 2007).…”

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confidence: 99%

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Identification of NCAM‐binding peptides promoting neurite outgrowth via a heterotrimeric G‐protein‐coupled pathway

Hansen¹,

Christensen²,

Korshunova³

et al. 2007

Journal of Neurochemistry

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A combinatorial library of undecapeptides was produced and utilized for the isolation of peptide binding to the fibronectin type 3 modules (F3I-F3II) of the neural cell adhesion molecule (NCAM). The isolated peptides were sequenced and produced as dendrimers. Two of the peptides (denoted EN-FIN2 and ENFIN11) were confirmed to bind to F3I-F3II of NCAM by surface plasmon resonance. The peptides induced neurite outgrowth in primary cerebellar neurons and PC12E2 cells, but had no apparent neuroprotective properties. NCAM is known to activate different intracellular pathways, including signaling through the fibroblast growth factor receptor, the Src-related non-receptor tyrosine kinase Fyn, and heterotrimeric G-proteins. Interestingly, neurite outgrowth stimulated by ENFIN2 and ENFIN11 was independent of signaling through fibroblast growth factor receptor and Fyn, but could be inhibited with pertussis toxin, an inhibitor of certain heterotrimeric G-proteins. Neurite outgrowth induced by trans-homophilic NCAM was unaffected by the peptides, whereas knockdown of NCAM completely abrogated ENFIN2-and ENFIN11-induced neuritogenesis. These observations suggest that ENFIN2 and ENFIN11 induce neurite outgrowth in an NCAM-dependent manner through G-protein-coupled signal transduction pathways. Thus, ENFIN2 and ENFIN11 may be valuable for exploring this particular type of NCAMmediated signaling.

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A novel splicing variation in L1CAM is responsible for recurrent fetal hydrocephalus

He,

Yao,

et al. 2023

Molec Gen & Gen Med

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BackgroundThe L1 cell adhesion molecule (L1CAM, OMIM 308840) gene is primarily expressed in the nervous system and encodes the L1 adhesion molecule protein. Variations in L1CAM cause a wide spectrum of X‐linked neurological disorders summarized as the L1 syndrome.MethodsWe report a 29‐year‐old pregnant woman who experienced multiple adverse pregnancy outcomes due to recurrent fetal hydrocephalus with an X‐linked recessive inheritance. Genomic DNA was extracted from the third aborted male fetus and analyzed via trio whole‐exome sequencing (WES). Total RNA was isolated from the pregnant woman to assess splicing variation at the mRNA level, and amniotic fluid was extracted from the woman for prenatal diagnosis on her fourth fetus.ResultsAll four male fetuses were affected by severe hydrocephalus. We identified a maternally derived hemizygous splicing variation NM_000425.5:[c.3046 + 1G > A]; NP_000416.1 p.(Gly1016AspfsTer6) (chrX:153130275) in Intron 22 of the L1CAM. This variation disrupts the donor splice site and causes the retention of Intron 22, which results in frame shift and a premature termination codon at position 1021 with the ability to produce a truncated protein without the fifth fibronectin‐repeat III, transmembrane, and cytoplasmic domains or to induce the degradation of mRNAs by nonsense‐mediated mRNA decay. The same hemizygous variant was also detected in the amniocytes.ConclusionThis report enhances our knowledge of genetic and phenotypic characteristics of X‐linked fetal hydrocephalus, providing a new genetic basis for prenatal diagnosis and pre‐implantation prenatal diagnosis.

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Cell Adhesion Molecules of the Immunoglobulin Superfamily in the Nervous System

Cited by 17 publications

References 781 publications

Characterization of BASP1‐mediated neurite outgrowth

Characterization of BASP1‐mediated neurite outgrowth

Identification of NCAM‐binding peptides promoting neurite outgrowth via a heterotrimeric G‐protein‐coupled pathway

A novel splicing variation in L1CAM is responsible for recurrent fetal hydrocephalus

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