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T-cell leukemia homeobox 1

HOX11, Hoxa2, HOXA11, TLX1
This gene encodes a nuclear transcription factor that belongs to the NK-linked or NK-like (NKL) subfamily of homeobox genes. The encoded protein is required for normal development of the spleen during embryogenesis. This protein is also involved in specification of neuronal cell fates. Ectopic expression of this gene due to chromosomal translocations is associated with certain T-cell acute lymphoblastic leukemias. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Sep 2010] (from NCBI)
Top mentioned proteins: CAN, HOX11L2, HOXA10, ACID, HOXA9
Papers using HOX11 antibodies
Targeting the NF-kappaB signaling pathway in Notch1-induced T-cell leukemia
Ferrando Adolfo A. et al., In Nature medicine, 2006
... TLX1-transgenic mice are polyclonal.
Inactivation of G2 checkpoint function and chromosomal destabilization are linked in human fibroblasts expressing human papillomavirus type 16 E6
Hough Margaret R et al., In Molecular Cancer, 1996
... stably expressing the HOX11 oncoprotein were generated by transfection of NIH 3T3 cultures with 3 μg MSCV-HOX11 plasmid constructs using the Polyfect Transfection reagent (QIAGEN), and selecting with 800 ...
Papers on HOX11
Regulation of inflammatory and angiogenesis mediators in a functional model of decidualized endometrial stromal cells.
Akoum et al., Québec, Canada. In Reprod Biomed Online, Jan 2016
Additionally, endometrial cells showed increased expression of homeobox HOXA10 and HOXA11 and LIFR, which are known to be involved in endometrial embryo receptivity.
Mutations in MECOM, Encoding Oncoprotein EVI1, Cause Radioulnar Synostosis with Amegakaryocytic Thrombocytopenia.
Aoki et al., Sendai, Japan. In Am J Hum Genet, Jan 2016
A heterozygous HOXA11 mutation has been identified in two unrelated families as a cause of RUSAT.
Analyses of fugu hoxa2 genes provide evidence for subfunctionalization of neural crest cell and rhombomere cis-regulatory modules during vertebrate evolution.
Krumlauf et al., Kansas City, United States. In Dev Biol, Dec 2015
Here we investigate the evolution of a Hoxa2 neural crest enhancer identified originally in mouse by comparing and contrasting the fugu hoxa2a and hoxa2b genes with their orthologous teleost and mammalian sequences.
Cryopreservation and recovery of human endometrial epithelial cells with high viability, purity, and functional fidelity.
Giudice et al., San Francisco, United States. In Fertil Steril, Nov 2015
Compared with eSF, recovered eECs displayed increased (P<.05) expression of epithelial-specific genes AREG, CDH1, DEFB4A, MMP7, and WNT7A, while exhibiting low-to-undetectable (P<.05) stromal-specific genes COL6A3, HOXA11, MMP2, PDGFRB, and WNT5A.
Molecular Analysis of the HOXA2-Dependent Degradation of RCHY1.
Rezsohazy et al., Louvain-la-Neuve, Belgium. In Plos One, 2014
The homeodomain transcription factor Hoxa2 interacts with the RING-finger type E3 ubiquitin ligase RCHY1 and induces its proteasomal degradation.
The Role of Hox Genes in Female Reproductive Tract Development, Adult Function, and Fertility.
Taylor et al., New Haven, United States. In Cold Spring Harb Perspect Med, 2014
Regulated HOXA10 and HOXA11 expression is necessary for endometrial receptivity; decreased HOXA10 or HOXA11 expression leads to decreased implantation rates.
Friend or foe: can activating mutations in NOTCH1 contribute to a favorable treatment outcome in patients with T-ALL?
Berger et al., Jerusalem, Israel. In Crit Rev Oncog, 2013
Transformation events occur during crucial steps of thymocyte development and have been related to the expression of certain oncogenes such as TAL2, TLX1, LYL1, LMO1, and NOTCH1.
Evolution of mammalian pregnancy and the origin of the decidual stromal cell.
Pavlicev et al., New Haven, United States. In Int J Dev Biol, 2013
Further support for this hypothesis is the origin of derived transcription factor interactions that are necessary for the regulation of decidual gene expression, in particular the interactions between HOXA11 and CEBPB with FOXO1A.
Tlx1/3 and Ptf1a control the expression of distinct sets of transmitter and peptide receptor genes in the developing dorsal spinal cord.
Cheng et al., Shanghai, China. In J Neurosci, 2012
Tlx1/3 and Ptf1a, the key transcription factors for fate determination of glutamatergic and GABAergic neurons in the dorsal spinal cord
TLX homeodomain oncogenes mediate T cell maturation arrest in T-ALL via interaction with ETS1 and suppression of TCRα gene expression.
Asnafi et al., France. In Cancer Cell, 2012
The cortical thymic maturation arrest in T-lineage Acute lymphoblastic leukemias (ALLs) that overexpress TLX1 or TLX3 is due to binding of TLX1/TLX3 to ETS1.
Hijacking T cell differentiation: new insights in TLX function in T-ALL.
Aifantis et al., New York City, United States. In Cancer Cell, 2012
TLX1 and TLX3 are two closely-related homeobox transcriptional repressors frequently misexpressed and translocated in T cell acute lymphoblastic leukemia (T-ALL).
Up-regulation of a HOXA-PBX3 homeobox-gene signature following down-regulation of miR-181 is associated with adverse prognosis in patients with cytogenetically abnormal AML.
Chen et al., Chicago, United States. In Blood, 2012
Data show that up-regulation of the HOXA7, HOXA9, HOXA11, and PBX3 resulting from the down-regulation of miR-181 family members probably contribute to the poor prognosis of patients with nonfavorable cytogenetically abnormal AML (CA-AML).
Reverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL.
Ferrando et al., New York City, United States. In Nat Med, 2012
these results place TLX1 and TLX3 at the top of an oncogenic transcriptional network controlling leukemia development, and identify RUNX1 as a tumor-suppressor gene in T-ALL
Expression of HOXA11 in the mid-luteal endometrium from women with endometriosis-associated infertility.
Jagodziński et al., Poznań, Poland. In Reprod Biol Endocrinol, 2011
reduced HOXA11 expression may contribute to endometriosis-associated infertility
The TLX1 oncogene drives aneuploidy in T cell transformation.
Ferrando et al., New York City, United States. In Nat Med, 2010
Transgenic expression of human TLX1 in mice induces T cell acute lymphoblastic leukemia with frequent deletions and mutations in Bcl11b.
Genetic rearrangements in relation to immunophenotype and outcome in T-cell acute lymphoblastic leukaemia.
Meijerink, Rotterdam, Netherlands. In Best Pract Res Clin Haematol, 2010
Mutually exclusive oncogenic rearrangements may delineate specific T-cell acute lymphoblastic leukaemia (T-ALL) subgroups, and so far at least 4 molecular-cytogenetic subgroups have been identified, i.e. the TAL/LMO, the TLX1/HOX11, the TLX3/HOX11L2 and the HOXA subgroups.
Deletion of the protein tyrosine phosphatase gene PTPN2 in T-cell acute lymphoblastic leukemia.
Cools et al., Leuven, Belgium. In Nat Genet, 2010
Deletion of PTPN2 was specifically found in T-ALLs with aberrant expression of the TLX1 transcription factor oncogene, including four cases also expressing the NUP214-ABL1 tyrosine kinase.
[HOX genes and the limb development in the clinical praxis and in the experiment].
Liska et al., In Cas Lek Cesk, 2009
In human, limb malformation was described in patients with mutations in HOXA11, HOXA13, HOXD10, and HOXD13 genes.
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