GFI1Growth Factor Independence 1
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In this study, we challenged Gfi1:GFP knock-in reporter mice by cecal ligation and puncture (CLP) surgery and found that the population of [CD11b.sup.+][Ly6G.sup.low][Ly6C.sup.high] cells in this sepsis model were heterogeneous and consisted of both monocytic and granulocytic MDSCs and that CD48 can distinguish monocytic and granulocytic MDSCs during infection.
Grimes, "Gfi1 regulates miR21 and miR-196b to control myelopoiesis," Blood, vol.
Genetic defects in severe congenital neutropenia Severe neutropenia Affected Characteristics type gene ELA2 deficiency ELA-2 AD or sporadic (OMIM: 202700) transmission HAX1 deficiency HAX-1 AR transmission, (OMIM: 610738) neurologic findings G6PC3 deficiency G6PC3 AR transmission, (OMIM: 611045) prominence in superficial veins, cardiac findings and urogenital anomalies X-linked neutropenia WAS X-linked transmission, (OMIM: 300392) T cell deficiency and natural killer cell deficiency may accompany GFI-1 deficiency GFI1 AD transmission, B and (OMIM: 600871) T lymphocyte deficiency may accompany ELA2: Neutrophil elastase, HAX1: HS1-related protein X-1, G6PC3: Glucose 6 phosphatase catalytic subunit 3, WAS: Wiskott-Aldrich syndrome, GFI-1: Growth factor independent-1 Table 2.
Mutations in proto oncogene GFI1 cause human neutropenia and target ELA2.
Similarly, in the GFI1 gene at Chr1:92947588, the mean read depth was 8.8[+ or -]8.8, with 26 individuals dropping out of the analysis.
Ikejiri et al., "PI3K-Akt-mTORC1-S6K1/2 axis controls Th17 differentiation by regulating Gfi1 expression and nuclear translocation of RORgamma," Cell Reports, vol.
The key role of ELANE in neutrophil homeostasis is also indicated by the development of SCN in patients carrying dominant negative mutations in the GFI1 gene,which is a transcriptional repressor of ELANE [92].
This is why, for the past 20 years, I have been studying a molecule called Gfi1, which plays an important role in the development of blood cells and cancer," Moroy said.
Gfi1. Gfi1 is another transcriptional regulator with important roles in DC development.
This approach used the most significant CpG from each of these three loci (AHRR, GFI1, and CYP1A1) from our genome-wide analysis and the corresponding robust linear regression coefficients to compute the smoking methylation score.
Other CpGs with prenatal smoke exposure-associated differential DNAm in the MoBa study were also significant at the strict look-up level (26 CpGs, p < 1.92 x [10.sup.-3]) in the SYS adolescents, including CpGs in CYP1A1, AHRR, and GFI1, and the gene-unmapped CpG 04598670 (Table 4).
We confirmed the 5 of 26 CpG sites (3 gene regions: AHRR, CYP1A1, and GFI1) that were additionally replicated (Bonferroni correction for 26 tests: p < 0.0019) by Joubert and colleagues using an independent population of infants born to 18 smoking and 18 nonsmoking mothers from the Newborn Epigenetics Study (NEST) (Figure 2A) (Joubert et al.