Clifford Woolf

Clifford Woolf, MB, BCh, PhD

Professor of Neurology, Harvard Medical School

Adaptive and Maladaptive Plasticity in Sensory and Motor Systems

Neurons are subject to functional, chemical and structural plasticity. This plasticity is an important factor both in the normal function of the nervous system and in a vast range of neurological diseases.

The Woolf lab studies how different forms of neuronal plasticity contribute both to adaptive and maladaptive changes in the mammalian nervous system, particularly in relation to pain, regeneration and neurodegenerative diseases.

Most of our work is concentrated on primary sensory and motor neurons, and to the interaction of neurons and immune cells, using a multidisciplinary approach spanning stem cell, molecular and cell biology, electrophysiology, neuroanatomy, behavior and genetics. We have established functional and comparative genomic strategies using expression profiling, bioinformatics and gain- and loss-of-function approaches, to screen for novel genes that contribute to neuronal plasticity and disease phenotypes. Our group works closely with many academic groups and the pharmaceutical industry to model disease and identify molecular targets for novel analgesics, axonal growth determinants and neuroprotective agents.

Current research includes study of the transcriptional control and post-translational processing of receptors and ion channels that mediate pain hypersensitivity, selective silencing of defined neuronal populations, intracellular signal transduction cascades activated by peripheral inflammation and nerve injury, neuro-immune interactions, transcription factors as master regulators of pain, growth and survival programs, cell survival in injured sensory and motor neurons, and the contribution of intrinsic growth determinants in establishing regenerative capacity in the peripheral and central nervous system. We are an active part of the Harvard Stem Cell Institute and are investigating how sensory and motor neurons reprogrammed from patient fibroblasts can be used to study pain and motor neuron disease and to screen for new treatments.

Publications View
Bone morphogenetic protein signaling by hemojuvelin regulates hepcidin expression.
Authors: Authors: Babitt JL, Huang FW, Wrighting DM, Xia Y, Sidis Y, Samad TA, Campagna JA, Chung RT, Schneyer AL, Woolf CJ, Andrews NC, Lin HY.
Nat Genet
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TRPA1 contributes to cold, mechanical, and chemical nociception but is not essential for hair-cell transduction.
Authors: Authors: Kwan KY, Allchorne AJ, Vollrath MA, Christensen AP, Zhang DS, Woolf CJ, Corey DP.
Neuron
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RNAi blocks DYT1 mutant torsinA inclusions in neurons.
Authors: Authors: Kock N, Allchorne AJ, Sena-Esteves M, Woolf CJ, Breakefield XO.
Neurosci Lett
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Runx1 determines nociceptive sensory neuron phenotype and is required for thermal and neuropathic pain.
Authors: Authors: Chen CL, Broom DC, Liu Y, de Nooij JC, Li Z, Cen C, Samad OA, Jessell TM, Woolf CJ, Ma Q.
Neuron
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Bradykinin and peripheral sensitization.
Authors: Authors: Wang H, Ehnert C, Brenner GJ, Woolf CJ.
Biol Chem
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The transcription factor ATF-3 promotes neurite outgrowth.
Authors: Authors: Seijffers R, Allchorne AJ, Woolf CJ.
Mol Cell Neurosci
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Detection of cold pain, cold allodynia and cold hyperalgesia in freely behaving rats.
Authors: Authors: Allchorne AJ, Broom DC, Woolf CJ.
Mol Pain
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Upregulation of the voltage-gated sodium channel beta2 subunit in neuropathic pain models: characterization of expression in injured and non-injured primary sensory neurons.
Authors: Authors: Pertin M, Ji RR, Berta T, Powell AJ, Karchewski L, Tate SN, Isom LL, Woolf CJ, Gilliard N, Spahn DR, Decosterd I.
J Neurosci
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Mutant SPTLC1 dominantly inhibits serine palmitoyltransferase activity in vivo and confers an age-dependent neuropathy.
Authors: Authors: McCampbell A, Truong D, Broom DC, Allchorne A, Gable K, Cutler RG, Mattson MP, Woolf CJ, Frosch MP, Harmon JM, Dunn TM, Brown RH.
Hum Mol Genet
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Role of the peripheral benzodiazepine receptor in sensory neuron regeneration.
Authors: Authors: Mills CD, Bitler JL, Woolf CJ.
Mol Cell Neurosci
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