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Cited by 83Protein Kinase Regulation and GTPase SignalingGenetics and Neurodevelopmental DisordersNeurogenesis and neuroplasticity mechanisms

Dock protein family in brain development and neurological disease

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Shi, Lei·2013·Communicative & Integrative Biology
DOI 10.4161/cib.26839PMC PMC3922786
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Abstract

The family of dedicator of cytokinesis (Dock), a protein family that belongs to the atypical Rho guanine nucleotide exchange factors (GEFs) for Rac and/or Cdc42 GTPases, plays pivotal roles in various processes of brain development. To date, 11 members of Docks have been identified in the mammalian system. Emerging evidence has suggested that members of the Dock family are associated with several neurodegenerative and neuropsychiatric diseases, including Alzheimer disease and autism spectrum disorders. This review summarizes recent advances on the understanding of the roles of the Dock protein family in normal and diseased processes in the nervous system. Furthermore, interacting proteins and the molecular regulation of Docks are discussed.

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  • DOCK2 expression is increased in the microglia of patients with AD.

    “Previous genetic studies have shown that DOCK4 variants are associated with multiple neurological phenotypes, and DOCK2, the other member of DOCK4’s protein subfamily, expression is increased in the microglia of patient’s with AD [49, 50].”

    From Multi-trait association studies discover pleiotropic loci between Alzheimer’s disease and cardiometabolic traits (2021) · cites this paper as [50]

    The Dock2 subsection reports that the number of DOCK2-expressing microglia is abnormally increased in the brains of patients with Alzheimer’s disease. It does not establish that DOCK2 expression is increased within individual microglial cells, as the claim could imply. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • DOCK families A and B contain N-terminal SH3 domains and a C-terminal proline-rich region that bind each other to maintain autoinhibition, which is alleviated upon binding adaptor proteins such as ELMO1.

    “Generally DOCK families A and B contain N-terminal SRC Homology 3 (SH3) domains and a C-terminal proline-rich region that bind each other to maintain the protein in an autoinhibited state, an interaction that is alleviated upon binding adaptor proteins such as engulfment and cell motility protein 1 (ELMO1) (36, 37).”

    From RHO to the DOCK for GDP disembarking: Structural insights into the DOCK GTPase nucleotide exchange factors (2021) · cites this paper as [36]

    The Introduction says Dock-A and Dock-B members have an N-terminal SH3 domain and a proline-rich C-terminus. The Regulation of Dock Activity section says ELMO binds the SH3 domain and releases Dock autoinhibition, but it does not say the SH3 domain and proline-rich region bind each other to maintain that state. No page numbers are available in our copy. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • The DOCK-D subfamily has roles in the immune system and neurology.

    “The DOCK-D subfamily, although not as well studied as other DOCKs, has been shown to have roles in the immune system and neurology (36, 48, 120).”

    From RHO to the DOCK for GDP disembarking: Structural insights into the DOCK GTPase nucleotide exchange factors (2021) · cites this paper as [36]

    The Dock-D section (page unavailable) says the subfamily is relatively less studied and reports neural roles for Dock9 and possible links between Dock9 and Dock10 and neurological conditions. It says Dock11 is expressed predominantly in lymphocytes, but does not establish an immune-system role for Dock-D members; that part of the claim is not supported by this copy. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • Previous genetic studies have shown that DOCK4 variants are associated with multiple neurological phenotypes.

    “Previous genetic studies have shown that DOCK4 variants are associated with multiple neurological phenotypes, and DOCK2, the other member of DOCK4’s protein subfamily, expression is increased in the microglia of patient’s with AD [49, 50].”

    From Multi-trait association studies discover pleiotropic loci between Alzheimer’s disease and cardiometabolic traits (2021) · cites this paper as [50]

  • DHR2 is responsible for binding and activation of RAC1.

    “the latter is responsible for binding and activation of RAC1 (Shi 2013).”

    From Heterozygous loss-of-function variants in DOCK4 cause neurodevelopmental delay and microcephaly (2024) · cites this paper as Shi 2013

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References 84 · Cited by 83

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Authors
Shi, L.
Affiliations
Jinan University (CN)
Corresponding author
Shi, Lei
ORCID
Shi, Lei
Venue
Communicative & Integrative Biology
Publisher
Informa UK Limited
Published
2013-11-09
Volume
6
Issue
6
Pages
e26839
ISSN
1942-0889 (ISSN-L)
DOI
10.4161/cib.26839
PMC
PMC3922786
OpenAlex
W1991201188
Cited by
83
References
84
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FWCI
0.31
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Communicative & Integrative Biology (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
RhoGEF, Rac GTPase, Cdc42 GTPase, brain development, neurodegenerative diseases, Alzheimer's disease, autism spectrum disorder, neuropsychiatric disorders, protein-protein interaction, molecular regulation

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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