Format

Send to:

Choose Destination
    • Showing Current items.

    Cdc42 cell division cycle 42 [ Mus musculus (house mouse) ]

    Gene ID: 12540, updated on 14-Oct-2021

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    CREG ameliorates the phenotypic switching of cardiac fibroblasts after myocardial infarction via modulation of CDC42.

    CREG ameliorates the phenotypic switching of cardiac fibroblasts after myocardial infarction via modulation of CDC42.
    Liu D, Tian X, Liu Y, Song H, Cheng X, Zhang X, Yan C, Han Y., Free PMC Article

    09/25/2021
    Congenital biliary atresia is correlated with disrupted cell junctions and polarity caused by Cdc42 insufficiency in the liver.

    Congenital biliary atresia is correlated with disrupted cell junctions and polarity caused by Cdc42 insufficiency in the liver.
    Zhou Y, Ji H, Xu Q, Zhang X, Cao X, Chen Y, Shao M, Wu Z, Zhang J, Lu C, Yang J, Shi Y, Bu H., Free PMC Article

    07/31/2021
    Cdc42 localized in the CatSper signaling complex regulates cAMP-dependent pathways in mouse sperm.

    Cdc42 localized in the CatSper signaling complex regulates cAMP-dependent pathways in mouse sperm.
    Luque GM, Xu X, Romarowski A, Gervasi MG, Orta G, De la Vega-Beltrán JL, Stival C, Gilio N, Dalotto-Moreno T, Krapf D, Visconti PE, Krapf D, Darszon A, Buffone MG.

    07/24/2021
    The Small GTPase Cdc42 Negatively Regulates the Formation of Neutrophil Extracellular Traps by Engaging Mitochondria.

    The Small GTPase Cdc42 Negatively Regulates the Formation of Neutrophil Extracellular Traps by Engaging Mitochondria.
    Tackenberg H, Möller S, Filippi MD, Laskay T., Free PMC Article

    07/3/2021
    Specific deletion of CDC42 in pancreatic beta cells attenuates glucose-induced insulin expression and secretion in mice.

    Specific deletion of CDC42 in pancreatic β cells attenuates glucose-induced insulin expression and secretion in mice.
    He XQ, Wang N, Zhao JJ, Wang D, Wang CJ, Xie L, Zheng HY, Shi SZ, He J, Zhou J, Xin HB, Deng KY.

    07/3/2021
    The dynactin subunit DCTN1 controls osteoclastogenesis via the Cdc42/PAK2 pathway.

    The dynactin subunit DCTN1 controls osteoclastogenesis via the Cdc42/PAK2 pathway.
    Lee YD, Kim B, Jung S, Kim H, Kim MK, Kwon JO, Song MK, Lee ZH, Kim HH., Free PMC Article

    07/3/2021
    Elevating EGFR-MAPK program by a nonconventional Cdc42 enhances intestinal epithelial survival and regeneration.

    Elevating EGFR-MAPK program by a nonconventional Cdc42 enhances intestinal epithelial survival and regeneration.
    Zhang X, Bandyopadhyay S, Araujo LP, Tong K, Flores J, Laubitz D, Zhao Y, Yap G, Wang J, Zou Q, Ferraris R, Zhang L, Hu W, Bonder EM, Kiela PR, Coffey R, Verzi MP, Ivanov II, Gao N., Free PMC Article

    06/12/2021
    Ror2-mediated non-canonical Wnt signaling regulates Cdc42 and cell proliferation during tooth root development.

    Ror2-mediated non-canonical Wnt signaling regulates Cdc42 and cell proliferation during tooth root development.
    Ma Y, Jing J, Feng J, Yuan Y, Wen Q, Han X, He J, Chen S, Ho TV, Chai Y., Free PMC Article

    04/24/2021
    The Small GTPase Cdc42 Is a Major Regulator of Neutrophil Effector Functions.

    The Small GTPase Cdc42 Is a Major Regulator of Neutrophil Effector Functions.
    Tackenberg H, Möller S, Filippi MD, Laskay T., Free PMC Article

    04/3/2021
    Rho-GEF trio regulates osteoclast differentiation and function by Rac1/Cdc42.

    Rho-GEF trio regulates osteoclast differentiation and function by Rac1/Cdc42.
    Gu J, Yang Z, Yuan L, Guo S, Wang D, Zhao N, Meng L, Liu H, Chen W, Ma J.

    03/13/2021
    Activation of FAK/Rac1/Cdc42-GTPase signaling ameliorates impaired microglial migration response to Abeta42 in triggering receptor expressed on myeloid cells 2 loss-of-function murine models.

    Activation of FAK/Rac1/Cdc42-GTPase signaling ameliorates impaired microglial migration response to Aβ<sub>42</sub> in triggering receptor expressed on myeloid cells 2 loss-of-function murine models.
    Rong Z, Cheng B, Zhong L, Ye X, Li X, Jia L, Li Y, Shue F, Wang N, Cheng Y, Huang X, Liu CC, Fryer JD, Wang X, Zhang YW, Zheng H.

    02/27/2021
    Neuropathophysiological significance of the c.1449T>C/p.(Tyr64Cys) mutation in the CDC42 gene responsible for Takenouchi-Kosaki syndrome.

    Neuropathophysiological significance of the c.1449T&gt;C/p.(Tyr64Cys) mutation in the CDC42 gene responsible for Takenouchi-Kosaki syndrome.
    Hamada N, Ito H, Shibukawa Y, Morishita R, Iwamoto I, Okamoto N, Nagata KI.

    02/13/2021
    miR-485-5p suppresses Schwann cell proliferation and myelination by targeting cdc42 and Rac1.

    miR-485-5p suppresses Schwann cell proliferation and myelination by targeting cdc42 and Rac1.
    Zhang Z, Li X, Li A, Wu G.

    10/31/2020
    Dopamine D1 and D2 Receptors Differentially Regulate Rac1 and Cdc42 Signaling in the Nucleus Accumbens to Modulate Behavioral and Structural Plasticity After Repeated Methamphetamine Treatment.

    Dopamine D<sub>1</sub> and D<sub>2</sub> Receptors Differentially Regulate Rac1 and Cdc42 Signaling in the Nucleus Accumbens to Modulate Behavioral and Structural Plasticity After Repeated Methamphetamine Treatment.
    Tu G, Ying L, Ye L, Zhao J, Liu N, Li J, Liu Y, Zhu M, Wu Y, Xiao B, Guo H, Guo F, Wang H, Zhang L, Zhang L.

    10/3/2020
    Rational targeting Cdc42 restrains Th2 cell differentiation and prevents allergic airway inflammation.

    Rational targeting Cdc42 restrains Th2 cell differentiation and prevents allergic airway inflammation.
    Yang JQ, Kalim KW, Li Y, Duan X, Nguyen P, Khurana Hershey GK, Kroner J, Ruff B, Zhang L, Salomonis N, Rochman M, Wen T, Zheng Y, Guo F., Free PMC Article

    09/26/2020
    Effects of age-dependent changes in cell size on endothelial cell proliferation and senescence through YAP1.

    Effects of age-dependent changes in cell size on endothelial cell proliferation and senescence through YAP1.
    Mammoto T, Torisawa YS, Muyleart M, Hendee K, Anugwom C, Gutterman D, Mammoto A., Free PMC Article

    09/5/2020
    Cdc42 Deficiency Leads To Epidermal Barrier Dysfunction by Regulating Intercellular Junctions and Keratinization of Epidermal Cells during Mouse Skin Development.

    Cdc42 Deficiency Leads To Epidermal Barrier Dysfunction by Regulating Intercellular Junctions and Keratinization of Epidermal Cells during Mouse Skin Development.
    Zhang M, Wang X, Guo F, Jia Q, Liu N, Chen Y, Yan Y, Huang M, Tang H, Deng Y, Huang S, Zhou Z, Zhang L, Zhang L., Free PMC Article

    08/22/2020
    The results indicate that SLIT2 inhibits osteoclastogenesis and the resultant bone resorption by decreasing Cdc42 activity, suggesting that this is a potential therapeutic target in metabolic bone diseases related to high bone turnover states.

    SLIT2 inhibits osteoclastogenesis and bone resorption by suppression of Cdc42 activity.
    Park SJ, Lee JY, Lee SH, Koh JM, Kim BJ.

    06/20/2020
    Knockdown of Cdc42, a Rho family protein, caused mislocalization of neonatal dentate granule cells, although the effects were moderate compared to Rac1 and 3. Despite the ectopic localization, Rac3- or Cdc42-disrupted mispositioned cells expressed Prox1.

    Rho family GTPases, Rac and Cdc42, control the localization of neonatal dentate granule cells during brain development.
    Ito H, Morishita R, Mizuno M, Tabata H, Nagata KI.

    06/6/2020
    activation of Cdc42 by endothelin signaling is important for cardiac neural crest cell migration in the outflow tract but this pathway is not involved in mandibular or pharyngeal arch artery patterning.

    Cdc42 activation by endothelin regulates neural crest cell migration in the cardiac outflow tract.
    Fritz KR, Zhang Y, Ruest LB.

    05/9/2020
    Here, the authors show that angiogenic collective endothelial cell migration is regulated by non-canonical Wnt signaling. They identify that Wnt5a specifically activates Cdc42 at cell junctions downstream of ROR2 to reinforce coupling between adherens junctions and the actin cytoskeleton.

    Non-canonical Wnt signaling regulates junctional mechanocoupling during angiogenic collective cell migration.
    Carvalho JR, Fortunato IC, Fonseca CG, Pezzarossa A, Barbacena P, Dominguez-Cejudo MA, Vasconcelos FF, Santos NC, Carvalho FA, Franco CA., Free PMC Article

    02/29/2020
    These results showed that loss of Cdc42 caused a defect of intramembranous ossification in cranial bone tissues which is related to decreased expressions of cranial suture morphogenesis genes, including Indian hedgehog and bone morphogenetic proteins.

    Cdc42 regulates cranial suture morphogenesis and ossification.
    Aizawa R, Yamada A, Seki T, Tanaka J, Nagahama R, Ikehata M, Kato T, Sakashita A, Ogata H, Chikazu D, Maki K, Mishima K, Yamamoto M, Kamijo R.

    02/8/2020
    endothelial-specific deletion of Cdc42 elicits CCM-like cerebrovascular malformations and that CDC42 is engaged in the cerebral cavernous malformation signaling network to restrain the MEKK3-MEK5-ERK5-KLF2/4 pathway.

    CDC42 Deletion Elicits Cerebral Vascular Malformations via Increased MEKK3-Dependent KLF4 Expression.
    Castro M, Laviña B, Ando K, Álvarez-Aznar A, Abu Taha A, Brakebusch C, Dejana E, Betsholtz C, Gaengel K.

    01/25/2020
    Cdc42 is apparently required for both articular cartilage degeneration and subchondral bone deterioration of osteoarthritis, thus, interventions targeting Cdc42 have potential in osteoarthritic therapy.

    Cdc42 Is Essential for Both Articular Cartilage Degeneration and Subchondral Bone Deterioration in Experimental Osteoarthritis.
    Hu X, Ji X, Yang M, Fan S, Wang J, Lu M, Shi W, Mei L, Xu C, Fan X, Hussain M, Du J, Wu J, Wu X.

    10/26/2019
    we have shown that two isoforms of Cdc42 gene with distinct functions in neuronal polarity are differentially localized between neurites and soma of mESC-derived and mouse primary cortical neurons, at both mRNA and protein level.

    Alternative 3' UTRs direct localization of functionally diverse protein isoforms in neuronal compartments.
    Ciolli Mattioli C, Rom A, Franke V, Imami K, Arrey G, Terne M, Woehler A, Akalin A, Ulitsky I, Chekulaeva M., Free PMC Article

    10/19/2019
    firstprevious page of 10 nextlast
    Support Center