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    RAC2 Rac family small GTPase 2 [ Homo sapiens (human) ]

    Gene ID: 5880, updated on 7-Jul-2019

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    We found both the rs229527 allele within C1QTNF6 (odds ratio [OR] = 1.23, confidence interval [95% CI]: 1.12-1.33, pAllelic = 4.60 . 10-6) and the rs2284038 allele within RAC2 (OR = 1.10, 95% CI: 1.01-0.19, pAllelic = 3.00 . 10-2) showed significant associations with Graves' Disease susceptibility.

    Association Analysis of Single Nucleotide Polymorphisms in C1QTNF6, RAC2, and an Intergenic Region at 14q32.2 with Graves' Disease in Chinese Han Population.
    Zhang XH, Shen M, Liu L, Li FM, Hu PC, Hua Q, Zhang J, Pang LN, Lu HW, Wang ZM, Chu X, Huang W.

    miR-24-1*/let-7a*-ARP2/3 complex-RAC isoforms pathway may represent a novel pathogenic mechanism for Hirschsprung disease.

    Suppressive action of miRNAs to ARP2/3 complex reduces cell migration and proliferation via RAC isoforms in Hirschsprung disease.
    Tang W, Cai P, Huo W, Li H, Tang J, Zhu D, Xie H, Chen P, Hang B, Wang S, Xia Y., Free PMC Article

    P38 MAPK, phosphorylated P38 MAPK, and RAC2 regulated in mutual feedback and negative feedback regulatory pathways, resulting in the radioresistance of G0 cells.

    RAC2-P38 MAPK-dependent NADPH oxidase activity is associated with the resistance of quiescent cells to ionizing radiation.
    Pei H, Zhang J, Nie J, Ding N, Hu W, Hua J, Hirayama R, Furusawa Y, Liu C, Li B, Hei TK, Zhou G., Free PMC Article

    Rac2 to modulates the level of Rac1-dependent macrophage IL-1beta expression, which consequently determines extent of atherosclerotic calcification.

    Rac2 Modulates Atherosclerotic Calcification by Regulating Macrophage Interleukin-1β Production.
    Ceneri N, Zhao L, Young BD, Healy A, Coskun S, Vasavada H, Yarovinsky TO, Ike K, Pardi R, Qin L, Qin L, Tellides G, Hirschi K, Meadows J, Soufer R, Chun HJ, Sadeghi MM, Bender JR, Morrison AR., Free PMC Article

    R665W and L845F be referred to as allomorphic rather than hypermorphic mutations of PLCG2 Rerouting of the transmembrane signals emanating from BCR and converging on PLCgamma2 through Rac in ibrutinib-resistant CLL cells may provide novel drug treatment strategies to overcome ibrutinib resistance mediated by PLCG2 mutations or to prevent its development in ibrutinib-treated CLL patients.

    The Phospholipase Cγ2 Mutants R665W and L845F Identified in Ibrutinib-resistant Chronic Lymphocytic Leukemia Patients Are Hypersensitive to the Rho GTPase Rac2 Protein.
    Walliser C, Hermkes E, Schade A, Wiese S, Deinzer J, Zapatka M, Désiré L, Mertens D, Stilgenbauer S, Gierschik P., Free PMC Article

    Study showed that RhoA/Rac2 participate in hepatocellular tumorigenesis through their upregulation by AFAP1-AS1.

    Long noncoding RNA AFAP1-AS1 indicates a poor prognosis of hepatocellular carcinoma and promotes cell proliferation and invasion via upregulation of the RhoA/Rac2 signaling.
    Zhang JY, Weng MZ, Song FB, Xu YG, Liu Q, Wu JY, Qin J, Jin T, Xu JM.

    RAC1/RAC2 and SFK are proximal and essential for phosphatidylinositol 3-kinase (PI3K) activation in NK cell-mediated direct cytotoxicity against Cryptococcus neoformans.

    Ras-related C3 Botulinum Toxin Substrate (Rac) and Src Family Kinases (SFK) Are Proximal and Essential for Phosphatidylinositol 3-Kinase (PI3K) Activation in Natural Killer (NK) Cell-mediated Direct Cytotoxicity against Cryptococcus neoformans.
    Xiang RF, Stack D, Huston SM, Li SS, Ogbomo H, Kyei SK, Mody CH., Free PMC Article

    RAC2 specifically interacted with a set of mitochondrial proteins.

    Mitochondrial Dysfunction in Human Leukemic Stem/Progenitor Cells upon Loss of RAC2.
    Capala ME, Maat H, Bonardi F, van den Boom V, Kuipers J, Vellenga E, Giepmans BN, Schuringa JJ., Free PMC Article

    our present analysis reinforces the involvement in ACT of the regulatory NADPH oxidase subunit RAC2 gene variant rs13058338 and, to a lesser extent of the CYBA gene variant rs4673.

    Association of NADPH oxidase polymorphisms with anthracycline-induced cardiotoxicity in the RICOVER-60 trial of patients with aggressive CD20(+) B-cell lymphoma.
    Reichwagen A, Ziepert M, Kreuz M, Gödtel-Armbrust U, Rixecker T, Poeschel V, Reza Toliat M, Nürnberg P, Tzvetkov M, Deng S, Trümper L, Hasenfuss G, Pfreundschuh M, Wojnowski L.

    homozygous loss-of-function RAC2 mutation in 2 patients with early-onset and progressive hypogammaglobulinemia(novel homozygous nonsense mutation in codon 56 (W56X)of RAC2 gene)

    RAC2 loss-of-function mutation in 2 siblings with characteristics of common variable immunodeficiency.
    Alkhairy OK, Rezaei N, Graham RR, Abolhassani H, Borte S, Hultenby K, Wu C, Aghamohammadi A, Williams DA, Behrens TW, Hammarström L, Pan-Hammarström Q., Free PMC Article

    p47(phox) and Rac2 accumulate only transiently at the phagosome at the onset of NADPH activity and detach from the phagosome before the end of reactive oxygen species production.

    The recruitment of p47(phox) and Rac2G12V at the phagosome is transient and phosphatidylserine dependent.
    Faure MC, Sulpice JC, Delattre M, Lavielle M, Prigent M, Cuif MH, Melchior C, Tschirhart E, Nüße O, Dupré-Crochet S.

    These studies imply functional importance of iNOS and its interaction with Rac2 in pathogen killing by the neutrophils.

    Interaction of inducible nitric oxide synthase with rac2 regulates reactive oxygen and nitrogen species generation in the human neutrophil phagosomes: implication in microbial killing.
    Jyoti A, Singh AK, Dubey M, Kumar S, Saluja R, Keshari RS, Verma A, Chandra T, Kumar A, Bajpai VK, Barthwal MK, Dikshit M.

    findings indicate that a chemokine-controlled pathway, consisting of Galphai2, ELMO1/Dock180, Rac1 and Rac2, regulates the actin cytoskeleton during breast cancer metastasis

    Association between Gαi2 and ELMO1/Dock180 connects chemokine signalling with Rac activation and metastasis.
    Li H, Yang L, Fu H, Yan J, Wang Y, Guo H, Hao X, Xu X, Jin T, Zhang N., Free PMC Article

    Mutations in hematopoiesis-specific Rho GTPases Rac2 and RhoH lead to a wide range of human blood disorders. (Review)

    Hematopoietic-specific Rho GTPases Rac2 and RhoH and human blood disorders.
    Troeger A, Williams DA., Free PMC Article

    study identified several missense mutations for RAC1 and RAC2, with some of the mutant proteins, including RAC1(P29S), RAC1(C157Y), RAC2(P29L), and RAC2(P29Q), being found to be activated and transforming; activating mutations of RAC GTPases were thus found in a wide variety of cancers at a low frequency

    Transforming mutations of RAC guanosine triphosphatases in human cancers.
    Kawazu M, Ueno T, Kontani K, Ogita Y, Ando M, Fukumura K, Yamato A, Soda M, Takeuchi K, Miki Y, Yamaguchi H, Yasuda T, Naoe T, Yamashita Y, Katada T, Choi YL, Mano H., Free PMC Article

    This variant reduced binding of the NCF2 gene product p67(phox) to RAC2. This study found a novel genetic association of RAC2 with Crohn's disease (CD) and replicated the previously reported association of NCF4 with ileal CD.

    NADPH oxidase complex and IBD candidate gene studies: identification of a rare variant in NCF2 that results in reduced binding to RAC2.
    Muise AM, Xu W, Guo CH, Walters TD, Wolters VM, Fattouh R, Lam GY, Hu P, Murchie R, Sherlock M, Gana JC, NEOPICS., Russell RK, Glogauer M, Duerr RH, Cho JH, Lees CW, Satsangi J, Wilson DC, Paterson AD, Griffiths AM, Silverberg MS, Brumell JH., Free PMC Article

    The mRNA and protein levels of Rac1 and Rac2 are elevated following exposure of endothelial progenitor cells to the chemokine SDF-1alpha.

    The role of SDF-1α/Rac pathway in the regulation of endothelial progenitor cell polarity; homing and expression of Rac1, Rac2 during endothelial repair.
    Shen L, Gao Y, Qian J, Wu Y, Zhou M, Sun A, Zou Y, Ge J.

    Rac2 GTPase alters mitochondrial membrane potential and electron flow through the mitochondrial respiratory chain complex III, generating high levels of reactive oxygen species in chronic-phase CML stem cells and primitive leukemia progenitor cells.

    Rac2-MRC-cIII-generated ROS cause genomic instability in chronic myeloid leukemia stem cells and primitive progenitors.
    Nieborowska-Skorska M, Kopinski PK, Ray R, Hoser G, Ngaba D, Flis S, Cramer K, Reddy MM, Koptyra M, Penserga T, Glodkowska-Mrowka E, Bolton E, Holyoake TL, Eaves CJ, Cerny-Reiterer S, Valent P, Hochhaus A, Hughes TP, van der Kuip H, Sattler M, Wiktor-Jedrzejczak W, Richardson C, Dorrance A, Stoklosa T, Williams DA, Skorski T., Free PMC Article

    data reinforce recent evidences that susceptibility alleles/haplotypes are shared among multiple autoimmune disorders and support a causal role for RAC2 variants in the pathogenesis of autoimmune diseases.

    An evolutionary analysis of RAC2 identifies haplotypes associated with human autoimmune diseases.
    Sironi M, Guerini FR, Agliardi C, Biasin M, Cagliani R, Fumagalli M, Caputo D, Cassinotti A, Ardizzone S, Zanzottera M, Bolognesi E, Riva S, Kanari Y, Miyazawa M, Clerici M.

    CNF1 modified Rac2, which then interacted with the innate immune adaptors IMD and Rip1-Rip2 in flies and mammalian cells, respectively, to drive an immune response

    Pathogen-derived effectors trigger protective immunity via activation of the Rac2 enzyme and the IMD or Rip kinase signaling pathway.
    Boyer L, Magoc L, Dejardin S, Cappillino M, Paquette N, Hinault C, Charriere GM, Ip WK, Fracchia S, Hennessy E, Erturk-Hasdemir D, Reichhart JM, Silverman N, Lacy-Hulbert A, Stuart LM., Free PMC Article

    Rac1 and Rac2 GTPases are essential for normal bone marrow erythropoiesis, but they are dispensable for erythropoiesis in the spleen.

    Rac1 and Rac2 GTPases are necessary for early erythropoietic expansion in the bone marrow but not in the spleen.
    Kalfa TA, Pushkaran S, Zhang X, Johnson JF, Pan D, Daria D, Geiger H, Cancelas JA, Williams DA, Zheng Y., Free PMC Article

    LFA-1-induced stabilization of ARE-containing mRNAs in T cells is dependent on HuR, and occurs through the Vav-1, Rac1/2, MKK3 and p38MAPK signaling cascade

    T cell LFA-1 engagement induces HuR-dependent cytokine mRNA stabilization through a Vav-1, Rac1/2, p38MAPK and MKK3 signaling cascade.
    Ramgolam VS, DeGregorio SD, Rao GK, Collinge M, Subaran SS, Markovic-Plese S, Pardi R, Bender JR., Free PMC Article

    activated cells PLD2 affects Rac2 in an initial positive feedback, but as Rac2-GTP accumulates in the cell, this constitutes a "termination signal" leading to PLD2 inactivation.

    Evidence for two CRIB domains in phospholipase D2 (PLD2) that the enzyme uses to specifically bind to the small GTPase Rac2.
    Peng HJ, Henkels KM, Mahankali M, Dinauer MC, Gomez-Cambronero J., Free PMC Article

    Mutations in RAC2 GTPase have been found to cause a human disease, a severe phagocytic immunodeficiency characterized by lifethreatening infections in infancy. Review.

    Rac GTPases in human diseases.
    Pai SY, Kim C, Williams DA., Free PMC Article

    Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)

    Polymorphisms in innate immunity genes and patients response to dendritic cell-based HIV immuno-treatment.
    Segat L, Brandão LAC, Guimarães RL, Pontillo A, Athanasakis E, de Oliveira RM, Arraes LC, de Lima Filho JL, Crovella S.

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