Kimberly Huber, Ph.D.

Professor

Endowed Title: Southwestern Medical Foundation Scholar in Medical Research

Department: Neuroscience

Graduate Programs: Neuroscience

Biography

Dr. Huber obtained her Ph.D. in Neurobiology in 1995 from The University of Texas Graduate School of Biomedical Sciences in Houston where she worked with Drs. Paul Kelly and Michael Mauk on the neurobiological mechanisms of learning and memory, specifically long-term changes in neuronal connections, termed synaptic plasticity. Dr. Huber performed her postdoctoral training with Dr. Mark Bear at the Howard Hughes Medical Institute and Brown University where she discovered novel mechanisms and forms of synaptic plasticity as well as demonstrated specific alterations in synaptic plasticity in a mouse model of Fragile X Syndrome, the most common genetic cause of human mental retardation and autism. Dr. Huber joined the faculty at UT Southwestern in 2001 where she is she is currently a Professor in the Department of Neuroscience and Southwestern Medical Foundation Endowed Scholar.

Research in the Huber lab is focused on understanding the cellular and molecular mechanisms of synapse and neural circuit development and plasticity as well as the role of genes implicated in human autism and intellectual disability in these processes.  To address these questions her lab utilizes state-of-the-art neurophysiology, imaging, biochemistry and molecular biology techniques in mice.  Her lab has discovered novel molecular mechanisms of synaptic plasticity as well as new functions and mechanisms for the Fragile X Mental Retardation gene 1 (Fmr1) in cortical synapse development and plasticity. Her work has led to a better understanding of the neurobiology of Fragile X Syndrome and autism as well as identified novel therapeutic strategies. 

Work is the Huber laboratory is supported by grants from the NIH, FRAXA Research Foundation, The Simons Foundation for Autism Research Initiative and The Hartwell Foundation.

Education

Undergraduate Stephen F Austin State University (1987)
Graduate School University of Texas Health Science Center-Houston (1995)

Research Interests

  • Cortical Synapse Development and Plasticity
  • Dendritic Translational Control
  • Metabotropic Glutamate Receptors
  • Neurobiological Basis of Fragile X Syndrome/Autism/Intellectual disability

Publications

Featured Publications Legend

Featured Publications

A Role for Dendritic mGluR5-Mediated Local Translation of Arc/Arg3.1 in MEF2-Dependent Synapse Elimination.

Wilkerson JR, Tsai NP, Maksimova MA, Wu H, Cabalo NP, Loerwald KW, Dictenberg JB, Gibson JR, Huber KM Cell Rep 2014 May

Postsynaptic FMRP Promotes the Pruning of Cell-to-Cell Connections among Pyramidal Neurons in the L5A Neocortical Network.

Patel AB, Loerwald KW, Huber KM, Gibson JR J. Neurosci. 2014 Feb 34 9 3413-8

Experience-Induced Arc/Arg3.1 Primes CA1 Pyramidal Neurons for Metabotropic Glutamate Receptor-Dependent Long-Term Synaptic Depression.

Jakkamsetti V, Tsai NP, Gross C, Molinaro G, Collins KA, Nicoletti F, Wang KH, Osten P, Bassell GJ, Gibson JR, Huber KM Neuron 2013 Oct 80 1 72-9

Postsynaptic FMRP bidirectionally regulates excitatory synapses as a function of developmental age and MEF2 activity.

Zang T, Maksimova MA, Cowan CW, Bassel-Duby R, Olson EN, Huber KM Mol. Cell. Neurosci. 2013 Mar

Multiple autism-linked genes mediate synapse elimination via proteasomal degradation of a synaptic scaffold PSD-95.

Tsai NP, Wilkerson JR, Guo W, Maksimova MA, DeMartino GN, Cowan CW, Huber KM Cell 2012 Dec 151 7 1581-94

Evidence for a fragile X mental retardation protein-mediated translational switch in metabotropic glutamate receptor-triggered Arc translation and long-term depression.

Niere F, Wilkerson JR, Huber KM J. Neurosci. 2012 Apr 32 17 5924-36

Disrupted Homer scaffolds mediate abnormal mGluR5 function in a mouse model of fragile X syndrome.

Ronesi JA, Collins KA, Hays SA, Tsai NP, Guo W, Birnbaum SG, Hu JH, Worley PF, Gibson JR, Huber KM Nat. Neurosci. 2012 Mar 15 3 431-40, S1

Altered neocortical rhythmic activity states in Fmr1 KO mice are due to enhanced mGluR5 signaling and involve changes in excitatory circuitry.

Hays SA, Huber KM, Gibson JR J. Neurosci. 2011 Oct 31 40 14223-34

Group 1 mGluR-dependent synaptic long-term depression: mechanisms and implications for circuitry and disease.

Lüscher C, Huber KM Neuron 2010 Feb 65 4 445-59

Protein translation in synaptic plasticity: mGluR-LTD, Fragile X.

Waung MW, Huber KM Curr. Opin. Neurobiol. 2009 Jun 19 3 319-26

Results 1-10 of 13

Honors/Awards

  • Simons Foundation Autism Research Initiative - Individual Investigator Award
    Simons Foundation (2012)
  • William and Enid Rosen Research Award for Outstanding Contributions to Fragile X Syndrome
    National Fragile X Foundation (2012)
  • Simons Foundation Autism Research Initiative -Pilot Award
    Simons Foundation (2009)
  • McKnight Foundation Brain Disorder Award
    (2002)
  • Endowed Scholars Award in Biomedical Research
    (2001)