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    KIF22 kinesin family member 22 [ Homo sapiens (human) ]

    Gene ID: 3835, updated on 17-Jun-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    KIF22 promotes multiple myeloma progression by regulating the CDC25C/CDK1/cyclinB1 pathway.

    KIF22 promotes multiple myeloma progression by regulating the CDC25C/CDK1/cyclinB1 pathway.
    Zhai M, Miao J, Zhang R, Liu R, Li F, Shen Y, Wang T, Xu X, Gao G, Hu J, He A, Bai J., Free PMC Article

    06/3/2024
    KIF22 promotes the proliferation and glycolysis of melanoma by activating EGFR/STAT3 signaling.

    KIF22 promotes the proliferation and glycolysis of melanoma by activating EGFR/STAT3 signaling.
    Zhong Z, Zhong H., Free PMC Article

    11/27/2023
    KIF22 Promotes Development of Pancreatic Cancer by Regulating the MEK/ERK/P21 Signaling Axis.

    KIF22 Promotes Development of Pancreatic Cancer by Regulating the MEK/ERK/P21 Signaling Axis.
    Zhang R, Ma L, Wei Y, Wei K, Song T, Du Z, Feng Z., Free PMC Article

    05/28/2022
    Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Tongue Squamous Cell Carcinoma.

    Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Tongue Squamous Cell Carcinoma.
    Liu Y, Li RH, Ren G, Jiang J., Free PMC Article

    11/28/2020
    Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Colon Cancer.

    Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Colon Cancer.
    Li B, Zhu FC, Yu SX, Liu SJ, Li BY.

    10/24/2020
    KIF22-dependent regulation of microtubule dynamics led to delayed EGFR internalization, enhanced EGFR signaling, and coordination of CAR dynamics at cell-cell junctions resulting in lung cancer.

    KIF22 coordinates CAR and EGFR dynamics to promote cancer cell proliferation.
    Pike R, Ortiz-Zapater E, Lumicisi B, Santis G, Parsons M., Free PMC Article

    07/6/2019
    We identified two candidate mutations in COL1A2 and MATN1, which might be affected by the main known mutation in B3GALT6. Our finding replicated a previously identified mutation in KIF22 to be potentially associated with spondyloepimetaphyseal dysplasia with joint laxity. We also show that our identified candidate mutation genes, COL1A2, MATN1 and KIF22, are in a direct biological interaction with B3GALT6.

    Detecting genetic modifiers of spondyloepimetaphyseal dysplasia with joint laxity in the Caucasian Afrikaner community.
    Chimusa ER, Beighton P, Kumuthini J, Ramesar RS.

    07/6/2019
    Chromokinesin Kid and kinetochore kinesin CENP-E differentially support chromosome congression without end-on attachment to microtubules.

    Chromokinesin Kid and kinetochore kinesin CENP-E differentially support chromosome congression without end-on attachment to microtubules.
    Iemura K, Tanaka K.

    02/20/2016
    we conclude that inhibition of KIF22 suppresses cancer cell proliferation by delaying mitotic exit through the transcriptional upregulation of CDC25C.

    Inhibition of KIF22 suppresses cancer cell proliferation by delaying mitotic exit through upregulating CDC25C expression.
    Yu Y, Wang XY, Sun L, Wang YL, Wan YF, Li XQ, Feng YM.

    08/9/2014
    Recurrent dominant mutations affecting two adjacent residues in the motor domain of the monomeric kinesin KIF22 result in skeletal dysplasia and joint laxity

    Recurrent dominant mutations affecting two adjacent residues in the motor domain of the monomeric kinesin KIF22 result in skeletal dysplasia and joint laxity.
    Boyden ED, Campos-Xavier AB, Kalamajski S, Cameron TL, Suarez P, Tanackovic G, Andria G, Ballhausen D, Briggs MD, Hartley C, Cohn DH, Davidson HR, Hall C, Ikegawa S, Jouk PS, König R, Megarbané A, Nishimura G, Lachman RS, Mortier G, Rimoin DL, Rogers RC, Rossi M, Sawada H, Scott R, Unger S, Valadares ER, Bateman JF, Warman ML, Superti-Furga A, Bonafé L., Free PMC Article

    02/4/2012
    Whole-exome sequencing identifies mutations of KIF22 in spondyloepimetaphyseal dysplasia with joint laxity, leptodactylic type

    Whole-exome sequencing identifies mutations of KIF22 in spondyloepimetaphyseal dysplasia with joint laxity, leptodactylic type.
    Min BJ, Kim N, Chung T, Kim OH, Nishimura G, Chung CY, Song HR, Kim HW, Lee HR, Kim J, Kang TH, Seo ME, Yang SD, Kim DH, Lee SB, Kim JI, Seo JS, Choi JY, Kang D, Kim D, Park WY, Cho TJ., Free PMC Article

    02/4/2012
    in all breast tumor tissues analyzed, variations in the Kid/KIF22 mRNA levels mirrored those seen with SIAH-1 mRNAs.

    Distinct expression patterns of the E3 ligase SIAH-1 and its partner Kid/KIF22 in normal tissues and in the breast tumoral processes.
    Bruzzoni-Giovanelli H, Fernandez P, Veiga L, Podgorniak MP, Powell DJ, Candeias MM, Mourah S, Calvo F, Marín M., Free PMC Article

    06/28/2010
    These data suggest that Kid-mediated anaphase/telophase chromosome compaction prevents formation of multinucleated cells.

    Kid-mediated chromosome compaction ensures proper nuclear envelope formation.
    Ohsugi M, Adachi K, Horai R, Kakuta S, Sudo K, Kotaki H, Tokai-Nishizumi N, Sagara H, Iwakura Y, Yamamoto T.

    01/21/2010
    Association of importin-beta and -alpha with hKid triggers the initial targeting of hKid to mitotic chromosomes; local Ran-GTP-mediated cargo release promotes the accumulation of hKid on chromosomes.

    Importin-beta and the small guanosine triphosphatase Ran mediate chromosome loading of the human chromokinesin Kid.
    Tahara K, Takagi M, Ohsugi M, Sone T, Nishiumi F, Maeshima K, Horiuchi Y, Tokai-Nishizumi N, Imamoto F, Yamamoto T, Kose S, Imamoto N., Free PMC Article

    01/21/2010
    human Aurora B and Kid are identified as APC/C(Cdh1) substrates

    Human Kid is degraded by the APC/C(Cdh1) but not by the APC/C(Cdc20).
    Feine O, Zur A, Mahbubani H, Brandeis M.

    01/21/2010
    its molecular structure and interaction with microtubules

    The second microtubule-binding site of monomeric kid enhances the microtubule affinity.
    Shiroguchi K, Ohsugi M, Edamatsu M, Yamamoto T, Toyoshima YY.

    01/21/2010
    These results suggest that distinct from its role in chromosome movement, Kid contributes to spindle morphogenesis by mediating spindle microtubules stabilization.

    The chromokinesin Kid is required for maintenance of proper metaphase spindle size.
    Tokai-Nishizumi N, Ohsugi M, Suzuki E, Yamamoto T., Free PMC Article

    01/21/2010
    These results are consistent with Kid having a role in chromosome congression in vivo, where it would be responsible for the polar ejection forces acting on the chromosome arms.

    The human chromokinesin Kid is a plus end-directed microtubule-based motor.
    Yajima J, Edamatsu M, Watai-Nishii J, Tokai-Nishizumi N, Yamamoto T, Toyoshima YY., Free PMC Article

    01/21/2010
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