PROTOGEL SAMPLE PREP KIT
- Known as:
- PROTOGEL SAMPLE PREP KIT
- Catalog number:
- EC-884-KIT
- Product Quantity:
- KIT
- Category:
- -
- Supplier:
- AGC
- Gene target:
- PROTOGEL SAMPLE PREP KIT
Related genes to: PROTOGEL SAMPLE PREP KIT
- Gene:
- PKNOX1 NIH gene
- Name:
- PBX/knotted 1 homeobox 1
- Previous symbol:
- -
- Synonyms:
- PREP1
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-03-19
- Date modifiied:
- 2015-09-04
- Gene:
- PREP NIH gene
- Name:
- prolyl endopeptidase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-12
- Date modifiied:
- 2016-10-05
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- Prep1, a TALE-family homeodomain transcription factor, has been demonstrated to play a critical role in embryonic hematopoiesis, as its insufficiency caused late embryonic lethality associated with defective hematopoiesis and angiogenesis. In the present study, we generated hematopoietic- and endothelial cell-specific Prep1-deficient mice and demonstrated that expression of Prep1 in the hematopoietic cell compartment is not essential for either embryonic or adult hematopoiesis, although its absence causes significant hematopoietic abnormalities in the adult bone marrow. Loss of Prep1 promotes cell cycling of hematopoietic stem/progenitor cells (HSPC), leading to the expansion of the HSPC pool. Prep1 deficiency also results in the accumulation of lineage-committed progenitors, increased monocyte/macrophage differentiation and arrested erythroid maturation. Maturation of T cells and B cells is also perturbed in Prep-deficient mice. These findings provide novel insight into the pleiotropic roles of Prep1 in adult hematopoiesis that were unrecognized in previous studies using germline Prep1 hypomorphic mice. - Source: PubMed
Publication date: 2015/08/18
Yoshioka KentaroOda AkihisaNotsu ChihiroOhtsuka TakafumiKawai YasuhiroSuzuki SadafumiNakamura TakuroMabuchi YoMatsuzaki YumiGoitsuka Ryo - The interactions of Meis, Prep, and Pbx1 TALE homeoproteins with Hox proteins are essential for development and disease. Although Meis and Prep behave similarly in vitro, their in vivo activities remain largely unexplored. We show that Prep and Meis interact with largely independent sets of genomic sites and select different DNA-binding sequences, Prep associating mostly with promoters and housekeeping genes and Meis with promoter-remote regions and developmental genes. Hox target sequences associate strongly with Meis but not with Prep binding sites, while Pbx1 cooperates with both Prep and Meis. Accordingly, Meis1 shows strong genetic interaction with Pbx1 but not with Prep1. Meis1 and Prep1 nonetheless coregulate a subset of genes, predominantly through opposing effects. Notably, the TALE homeoprotein binding profile subdivides Hox clusters into two domains differentially regulated by Meis1 and Prep1. During evolution, Meis and Prep thus specialized their interactions but maintained significant regulatory coordination. - Source: PubMed
Publication date: 2013/04/18
Penkov DmitryMateos San Martín DanielFernandez-Díaz Luis CRosselló Catalina ATorroja CarlosSánchez-Cabo FátimaWarnatz H JSultan MarcYaspo Marie LGabrieli AriannaTkachuk VsevolodBrendolan AndreaBlasi FrancescoTorres Miguel - Three amino acid loop extension (TALE) homeodomain-containing transcription factors are generally recognized for their role in organogenesis and differentiation during embryogenesis. However, very little is known about the expression and function of Meis, Pbx, and Prep genes during early development. - Source: PubMed
Publication date: 2012/10/10
Sonnet WendyRezsöhazy ReneDonnay Isabelle - Pax6 is an essential transcription factor for lens, lacrimal gland and pancreas development. Previous transgenic analyses have identified several Pax6 regulatory elements, but their functional significance and binding factors remain largely unknown. In this study, we generated two genomic truncations to delete three elements that were previously shown to bind to the Meis/Prep family homeoproteins. One 3.1 kb deletion (Pax6(∆DP/∆DP)) removed two putative pancreatic enhancers and a previously identified ectodermal enhancer, while a 450 bp sub-deletion (Pax6(∆PE/∆PE)) eliminated only the promoter-proximal pancreatic enhancer. Immunohistochemistry and quantitative RT-PCR showed that the Pax6(∆PE/∆PE) pancreata had a significant decrease in Pax6, glucagon, and insulin expression, while no further reductions were observed in the Pax6(∆DP/∆DP) mice, indicating that only the 450 bp region is required for pancreatic development. In contrast, Pax6(∆DP/∆DP), but not Pax6(∆PE/∆PE) mice, developed stunted lacrimal gland and lens hypoplasia which was significantly more severe than that reported when only the ectodermal enhancer was deleted. This result suggested that the ectodermal enhancer must cooperate with its neighboring sequences to regulate the Pax6 ectodermal expression. Finally, we generated conditional knockouts of Prep1 in the lens and pancreas, but surprisingly, did not observe any developmental defects. Together, these results provide functional evidence for the independent and synergistic roles of the Pax6 upstream enhancers, and they suggest the potential redundancy of Meis/Prep protein in Pax6 regulation. - Source: PubMed
Publication date: 2012/01/03
Carbe ChristianHertzler-Schaefer KristinaZhang Xin - Alterations in androgen levels lead to reproductive defects in both males and females, including hypogonadotropic hypogonadism, anovulation, and infertility. Androgens have been shown to down-regulate GnRH mRNA levels through an androgen receptor (AR)-dependent mechanism. Here, we investigate how androgen regulates expression from the GnRH regulatory region in the GT1-7 cell line, a model of GnRH neurons. A synthetic androgen, R1881, repressed transcription from the GnRH promoter (GnRH-P) in an AR-dependent manner, and liganded AR associated with the chromatin at the GnRH-P in live GT1-7 cells. The three known octamer-binding transcription factor-1 (Oct-1) binding sites in GnRH-P were required for AR-mediated repression, although other sequences were also involved. Although a multimer of the consensus Oct-1 binding site was not repressed, a multimer of the cluster of Oct-1, Pre-B cell leukemia transcription factor (Pbx)/Prep, and NK2 homeobox 1 (Nkx2.1) binding sites, found at -106/-91 in GnRH-P, was sufficient for repression. In fact, overexpression of any of these factors disrupted the androgen response, indicating that a balance of factors in this tripartite complex is required for AR repression. AR bound to this region in EMSA, indicating a direct interaction of AR with DNA or with other transcription factors bound to GnRH-P at this sequence. Collectively, our data demonstrate that GnRH transcription is repressed by AR via multiple sequences in GnRH-P, including three Oct-1 binding sites, and that this repression requires the complex interaction of several transcription factors. - Source: PubMed
Publication date: 2011/11/10
Brayman Melissa JPepa Patricia ABerdy Sara EMellon Pamela L