CBL-B functions as a negative regulator of
T-cell activation.[7] CBL-B expression in T cells causes ligand-induced T cell receptor down-modulation, controlling the activation degree of T cells during antigen presentation.[8][9]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Keane MM, Rivero-Lezcano OM, Mitchell JA, Robbins KC, Lipkowitz S (July 1995). "Cloning and characterization of cbl-b: a SH3 binding protein with homology to the c-cbl proto-oncogene". Oncogene. 10 (12): 2367–77.
PMID7784085.
^Naramura M, Jang IK, Kole H, Huang F, Haines D, Gu H (August 2002). "Pc-Cbl and Cbl-b regulate T cell responsiveness by promoting ligand-induced TCR down-modulation". Nature Immunology. 3 (12): 1192–9.
doi:
10.1038/ni855.
PMID12415267.
S2CID13354434.
^Yokoi N, Fujiwara Y, Wang HY, Kitao M, Hayashi C, Someya T, Kanamori M, Oiso Y, Tajima N, Yamada Y, Seino Y, Ikegami H, Seino S (March 2008). "Identification and functional analysis of CBLB mutations in type 1 diabetes". Biochem. Biophys. Res. Commun. 368 (1): 37–42.
doi:
10.1016/j.bbrc.2008.01.032.
PMID18201552.
Fang N, Fang D, Wang HY, et al. (2002). "Regulation of immune responses by E3 ubiquitin-protein ligases". In Altman A (ed.). Signal Transduction Pathways in Autoimmunity. Current Directions in Autoimmunity. Vol. 5. pp. 161–75.
doi:
10.1159/000060552.
ISBN3-8055-7308-1.
PMID11826757.
Ohira M, Morohashi A, Nakamura Y, et al. (2003). "Neuroblastoma oligo-capping cDNA project: toward the understanding of the genesis and biology of neuroblastoma". Cancer Lett. 197 (1–2): 63–8.
doi:
10.1016/S0304-3835(03)00085-5.
PMID12880961.
Fang D, Liu YC (2001). "Proteolysis-independent regulation of PI3K by Cbl-b-mediated ubiquitination in T cells". Nat. Immunol. 2 (9): 870–5.
doi:
10.1038/ni0901-870.
PMID11526404.
S2CID23051632.
CBL-B functions as a negative regulator of
T-cell activation.[7] CBL-B expression in T cells causes ligand-induced T cell receptor down-modulation, controlling the activation degree of T cells during antigen presentation.[8][9]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Keane MM, Rivero-Lezcano OM, Mitchell JA, Robbins KC, Lipkowitz S (July 1995). "Cloning and characterization of cbl-b: a SH3 binding protein with homology to the c-cbl proto-oncogene". Oncogene. 10 (12): 2367–77.
PMID7784085.
^Naramura M, Jang IK, Kole H, Huang F, Haines D, Gu H (August 2002). "Pc-Cbl and Cbl-b regulate T cell responsiveness by promoting ligand-induced TCR down-modulation". Nature Immunology. 3 (12): 1192–9.
doi:
10.1038/ni855.
PMID12415267.
S2CID13354434.
^Yokoi N, Fujiwara Y, Wang HY, Kitao M, Hayashi C, Someya T, Kanamori M, Oiso Y, Tajima N, Yamada Y, Seino Y, Ikegami H, Seino S (March 2008). "Identification and functional analysis of CBLB mutations in type 1 diabetes". Biochem. Biophys. Res. Commun. 368 (1): 37–42.
doi:
10.1016/j.bbrc.2008.01.032.
PMID18201552.
Fang N, Fang D, Wang HY, et al. (2002). "Regulation of immune responses by E3 ubiquitin-protein ligases". In Altman A (ed.). Signal Transduction Pathways in Autoimmunity. Current Directions in Autoimmunity. Vol. 5. pp. 161–75.
doi:
10.1159/000060552.
ISBN3-8055-7308-1.
PMID11826757.
Ohira M, Morohashi A, Nakamura Y, et al. (2003). "Neuroblastoma oligo-capping cDNA project: toward the understanding of the genesis and biology of neuroblastoma". Cancer Lett. 197 (1–2): 63–8.
doi:
10.1016/S0304-3835(03)00085-5.
PMID12880961.
Fang D, Liu YC (2001). "Proteolysis-independent regulation of PI3K by Cbl-b-mediated ubiquitination in T cells". Nat. Immunol. 2 (9): 870–5.
doi:
10.1038/ni0901-870.
PMID11526404.
S2CID23051632.