[No authors listed]
Monosomy 7 and interstitial deletion of 7q (-7/7q-) are well-recognized nonrandom chromosomal abnormalities frequently found among patients with myelodysplastic syndromes (MDSs) and myeloid leukemias. We previously identified candidate myeloid tumor suppressor genes (SAMD9, SAMD9-like = SAMD9L, and Miki) in the 7q21.3 subband. We established SAMD9L-deficient mice and found that SAMD9L(+/-) mice as well as SAMD9L(-/-) mice develop myeloid diseases resembling human diseases associated with -7/7q-. SAMD9L-deficient hematopoietic stem cells showed enhanced colony formation potential and in vivo reconstitution ability. SAMD9L localizes in early endosomes. SAMD9L-deficient cells showed delays in homotypic endosome fusion, resulting in persistence of ligand-bound cytokine receptors. These findings suggest that haploinsufficiency of SAMD9L and/or SAMD9 gene(s) contributes to myeloid transformation.
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Gm13242, Papd4, Wdr7, Ly76, Pld4, Ston2, Krt75, Slc8a3, Vmn1r13, Krtap5-5, Cebpd, Eef2, Muc4, Gsr, Ptpn6, Hoxb3, Itgam, Itgb3, Kcnab2, Lamp1, Vmn1r214, Pdgfra, Pdgfrb, Sirpa, Ptprc, Ptprz1, Rbmy, Rest, Sin3a, Serpinb9f, Samd9l, Dhtkd1, Mmp21, Eea1, Thy1, 4930474N05Rik, Arl11, Top2a, Prrc2c, Ppp4r2, Tcaf2, Ptprq, Bves, Muc19, Dact2, Wdr78, Siglecg, Rbm47, Zbtb24, Rab5a, Tmem91, Abca15, 6330408A02Rik, Dock1, Kcp, Mrgprx1, Agpat5, Arhgef7, Vmn2r74, Srsf4, Tnfrsf13b, Smpd3, Rrs1, Heatr9, Zfp784, Slc7a6os, Gpatch4, Acp6, Herc6, Dock7, Narfl, 4930430F08Rik, Eml1, Hrnr, Anln, Cyp2c66, Tmem143, 3830403N18Rik, Col24a1, Serpinb12, Esco2, Pygo1, Ssbp3, Sipa1l3, Wdr38, Armc6, Tmem190, Apobec3, SAMD9, EEA1
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