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    Dlx1 distal-less homeobox 1 [ Mus musculus (house mouse) ]

    Gene ID: 13390, updated on 27-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Dlx1/2-dependent expression of Meis2 promotes neuronal fate determination in the mammalian striatum.

    Dlx1/2-dependent expression of Meis2 promotes neuronal fate determination in the mammalian striatum.
    Su Z, Wang Z, Lindtner S, Yang L, Shang Z, Tian Y, Guo R, You Y, Zhou W, Rubenstein JL, Yang Z, Zhang Z., Free PMC Article

    03/12/2022
    Satb2 regulates the development of dopaminergic neurons in the arcuate nucleus by Dlx1.

    Satb2 regulates the development of dopaminergic neurons in the arcuate nucleus by Dlx1.
    Zhang Q, Zhang L, Huang Y, Ma P, Mao B, Ding YQ, Song NN., Free PMC Article

    02/5/2022
    Dlx1/2 mice have abnormal enteric nervous system function.

    Dlx1/2 mice have abnormal enteric nervous system function.
    Wright CM, Garifallou JP, Schneider S, Mentch HL, Kothakapa DR, Maguire BA, Heuckeroth RO., Free PMC Article

    05/29/2021
    Defining compartmentalized stem cell populations with distinct cell division dynamics in the ocular surface epithelium.

    Defining compartmentalized stem cell populations with distinct cell division dynamics in the ocular surface epithelium.
    Ishii R, Yanagisawa H, Sada A., Free PMC Article

    02/2/2021
    Dlx1/2 are Central and Essential Components in the Transcriptional Code for Generating Olfactory Bulb Interneurons.

    Dlx1/2 are Central and Essential Components in the Transcriptional Code for Generating Olfactory Bulb Interneurons.
    Guo T, Liu G, Du H, Wen Y, Wei S, Li Z, Tao G, Shang Z, Song X, Zhang Z, Xu Z, You Y, Chen B, Rubenstein JL, Yang Z., Free PMC Article

    10/24/2020
    Dlx1 and Dlx2 promote interneuron GABA synthesis, synaptogenesis, and dendritogenesis. Dlx1&2 coordinate key components of cortical interneurons postnatal development by promoting their excitability, inhibitory output, and survival.

    Dlx1 and Dlx2 Promote Interneuron GABA Synthesis, Synaptogenesis, and Dendritogenesis.
    Pla R, Stanco A, Howard MA, Rubin AN, Vogt D, Mortimer N, Cobos I, Potter GB, Lindtner S, Price JD, Nord AS, Visel A, Schreiner CE, Baraban SC, Rowitch DH, Rubenstein JLR., Free PMC Article

    12/21/2019
    Studies revealed that Dlx1/2 and Otp are required for the specification of growth hormone-releasing hormone (GHRH)- and AgRP-neurons, respectively. Dlx1/2 suppress agouti-related protein (AgRP)-neuronal fate by directly binding and repressing the Otp gene, uncovering a novel Dlx1/2-Otp gene regulatory axis critical for the segregation of GHRH- and AgRP-neuronal fates.

    Dlx1/2 and Otp coordinate the production of hypothalamic GHRH- and AgRP-neurons.
    Lee B, Kim J, An T, Kim S, Patel EM, Raber J, Lee SK, Lee S, Lee JW., Free PMC Article

    12/22/2018
    GABA is the major inhibitory neurotransmitter in the brain. We show that Dlx1/Dlx2 homeobox genes regulate GABA synthesis during forebrain development through direct activation of glutamic acid decarboxylase enzyme isoforms that convert glutamate to GABA.

    GABAergic Interneuron Differentiation in the Basal Forebrain Is Mediated through Direct Regulation of Glutamic Acid Decarboxylase Isoforms by Dlx Homeobox Transcription Factors.
    Le TN, Zhou QP, Cobos I, Zhang S, Zagozewski J, Japoni S, Vriend J, Parkinson T, Du G, Rubenstein JL, Eisenstat DD., Free PMC Article

    09/30/2017
    Dlx1 and Dlx2 function both downstream of ATOH7 and in parallel, but cooperative, pathways that involve regulation of Brn3b expression to determine retinal ganglion cell fate.

    Regulation of Brn3b by DLX1 and DLX2 is required for retinal ganglion cell differentiation in the vertebrate retina.
    Zhang Q, Zagozewski J, Cheng S, Dixit R, Zhang S, de Melo J, Mu X, Klein WH, Brown NL, Wigle JT, Schuurmans C, Eisenstat DD., Free PMC Article

    09/16/2017
    Dlx1 specifically suppresses Npn-2 and PAK3 and induces characteristic morphology of interneuron dendrites.

    Dlx1 transcription factor regulates dendritic growth and postsynaptic differentiation through inhibition of neuropilin-2 and PAK3 expression.
    Dai X, Iwasaki H, Watanabe M, Okabe S.

    10/4/2014
    despite their redundant properties, Gsx1 and -2 have distinct interactions with Dlx1 and -2

    Loss of Gsx1 and Gsx2 function rescues distinct phenotypes in Dlx1/2 mutants.
    Wang B, Long JE, Flandin P, Pla R, Waclaw RR, Campbell K, Rubenstein JL., Free PMC Article

    08/31/2013
    Mice devoid of Dlx1as RNA are viable and fertile, and display a mild skeletal and neurological phenotype of a Dlx1 gain-of function phenotype, suggesting a role for this non-coding antisense RNA in modulating Dlx1 transcript levels and stability

    Making sense of Dlx1 antisense RNA.
    Kraus P, Sivakamasundari V, Lim SL, Xing X, Lipovich L, Lufkin T.

    05/18/2013
    The functions of Dlx1 and Dlx2 are crucial for the initial formation of the posterior palatal shelves, and that the Dlx genes lie upstream of multiple signaling molecules and transcription factors important for later stages of palatogenesis.

    Cleft palate defect of Dlx1/2-/- mutant mice is caused by lack of vertical outgrowth in the posterior palate.
    Jeong J, Cesario J, Zhao Y, Burns L, Westphal H, Rubenstein JL., Free PMC Article

    03/23/2013
    mice with a conditional deletion of Dlx1 have a chronic reduction in inhibition that reduces receptive field size in mouse auditory cortex

    Chronic reduction in inhibition reduces receptive field size in mouse auditory cortex.
    Seybold BA, Stanco A, Cho KK, Potter GB, Kim C, Sohal VS, Rubenstein JL, Schreiner CE., Free PMC Article

    11/3/2012
    A subtype-specific reduction of interneurons, particularly in the superficial layers, is found in the visual cortex of Dlx1 mutant mice; however, there is no evidence for altered properties of thalamic relay to visual cortex in Dlx1 mutant mice.

    Influence of a subtype of inhibitory interneuron on stimulus-specific responses in visual cortex.
    Mao R, Schummers J, Knoblich U, Lacey CJ, Van Wart A, Cobos I, Kim C, Huguenard JR, Rubenstein JL, Sur M., Free PMC Article

    11/3/2012
    Voltage-clamp recordings of interneurons in hippocampal slices prepared from Dlx1-deficient animals older than postnatal day 30 reveal significant reduction in excitatory postsynaptic current amplitude.

    Deletion of Dlx1 results in reduced glutamatergic input to hippocampal interneurons.
    Jones DL, Howard MA, Stanco A, Rubenstein JL, Baraban SC., Free PMC Article

    04/21/2012
    Brn-3b suppresses the role of DLX1/2 through physical interaction and biases the competent precursors toward retinal ganglion cell fates.

    Brn-3b inhibits generation of amacrine cells by binding to and negatively regulating DLX1/2 in developing retina.
    Feng L, Eisenstat DD, Chiba S, Ishizaki Y, Gan L, Shibasaki K.

    02/11/2012
    These analyses define core transcriptional components that differentially specify the identity and differentiation of the globus pallidus, basal telencephalon, and pallial interneurons.

    Dlx1&2 and Mash1 transcription factors control MGE and CGE patterning and differentiation through parallel and overlapping pathways.
    Long JE, Cobos I, Potter GB, Rubenstein JL., Free PMC Article

    01/21/2010
    Data show that Cre-recombinase is active in a "Dlx-pattern" in the embryonic forebrain of transgenic mice, and suggest that both I12b and URE2 are direct targets of DLX2 and require Dlx1 and Dlx2 expression for proper activity.

    Generation of Cre-transgenic mice using Dlx1/Dlx2 enhancers and their characterization in GABAergic interneurons.
    Potter GB, Petryniak MA, Shevchenko E, McKinsey GL, Ekker M, Rubenstein JL., Free PMC Article

    01/21/2010
    Results identify Dlx-dependent and Dlx-independent pathways, and show that the Dlx-independent pathway depends in part on the function of the Mash1 b-HLH transcription factor.

    Dlx1&2 and Mash1 transcription factors control striatal patterning and differentiation through parallel and overlapping pathways.
    Long JE, Swan C, Liang WS, Cobos I, Potter GB, Rubenstein JL., Free PMC Article

    01/21/2010
    DLX proteins the potential to stimulate osteoblastic differentiation and may compensate for the absence of this protein to produce normal osteoblastic differentiation in knockout mice.

    Expression and function of Dlx genes in the osteoblast lineage.
    Li H, Marijanovic I, Kronenberg MS, Erceg I, Stover ML, Velonis D, Mina M, Heinrich JG, Harris SE, Upholt WB, Kalajzic I, Lichtler AC., Free PMC Article

    01/21/2010
    Dlx1&2 negatively regulate Olig2-dependant oligodendrocyte precursor cell formation. Role for Dlx genes as modulators of neuron versus oligodendrocyte development in ventral embryonic forebrain.

    Dlx1 and Dlx2 control neuronal versus oligodendroglial cell fate acquisition in the developing forebrain.
    Petryniak MA, Potter GB, Rowitch DH, Rubenstein JL., Free PMC Article

    01/21/2010
    DLX1 or DLX2 can function as transcriptional repressors

    Dlx homeobox genes promote cortical interneuron migration from the basal forebrain by direct repression of the semaphorin receptor neuropilin-2.
    Le TN, Du G, Fonseca M, Zhou QP, Wigle JT, Eisenstat DD.

    01/21/2010
    These data suggest that interneuron subtypes use distinct combinations of Dlx1/Dlx2 enhancers from the time they are specified through adulthood.

    Distinct cis-regulatory elements from the Dlx1/Dlx2 locus mark different progenitor cell populations in the ganglionic eminences and different subtypes of adult cortical interneurons.
    Ghanem N, Yu M, Long J, Hatch G, Rubenstein JL, Ekker M., Free PMC Article

    01/21/2010
    While Mash1 is required for early neurogenesis (E10.5), Dlx1 and Dlx2 are required to downregulate Notch signaling during specification and differentiation steps of 'late' progenitors (P3).

    Modulation of the notch signaling by Mash1 and Dlx1/2 regulates sequential specification and differentiation of progenitor cell types in the subcortical telencephalon.
    Yun K, Fischman S, Johnson J, Hrabe de Angelis M, Weinmaster G, Rubenstein JL.

    01/21/2010
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