Professor, Neurology, Wayne State University School of Medicine
Neurology
Dr. John A. Kamholz, MD
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Dr. John A. Kamholz works in the field of Neurology. He went to medical school at Perelman School of Medicine at the University of Pennsylvania. John A. Kamholz is a published physician. He published 72 publications, including: 'MEBA derepresses the proximal myelin basic protein promoter in oligodendrocytes.' John Kamholz accepts Medicare payments and is registered with Medicare.gov.
Publications
- Coexistence of a T118M PMP22 missense mutation and chromosome 17 (17p11.2-p12) deletion.
- Diffusion tensor imaging of patients with proteolipid protein 1 gene mutations.
- Neuroradiologic correlates of clinical disability and progression in the X-Linked leukodystrophy Pelizaeus-Merzbacher Disease.
- Curcumin derivatives promote Schwann cell differentiation and improve Neuropathy in R98C CMT1B mice.
- Neuronal cell injury precedes Brain atrophy in multiple sclerosis.
- Transient central Nervous system white matter abnormality in X-linked Charcot-Marie-Tooth disease.
- Differential regulation of the 2',3'-cyclic nucleotide 3'-phosphodiesterase gene during oligodendrocyte development.
- A minimal human MBP promoter-lacZ transgene is appropriately regulated in developing Brain and after optic enucleation, but not in shiverer mutant mice.
- Transcriptional regulation of the rat PLP promoter in primary cultures of oligodendrocytes.
- Organization and expression of the human myelin basic protein gene.
- Beta 4 integrin expression in myelinating Schwann cells is polarized, developmentally regulated and axonally dependent.
- Axons modulate the expression of transforming growth factor-betas in Schwann cells.
- Expression of growth-associated protein-43 kD in Schwann cells is regulated by axon-Schwann cell interactions and cAMP.
- Chickenpox with delayed contralateral hemiparesis caused by Cerebral angiitis.
- MEBA derepresses the proximal myelin basic protein promoter in oligodendrocytes.
- Oligodendrocyte maturation and myelin gene expression in PDGF-treated cultures from rat Cerebral white matter.
- TGFbeta1 modulates the phenotype of Schwann cells at the transcriptional level.
- Expression of P0 protein mRNA along rat sciatic Nerve during development.
- Developmental expression of P0 mRNA and P0 protein in the sciatic Nerve and the spinal Nerve roots of the rat.
- Mitogen-expanded Schwann cells retain the capacity to myelinate regenerating axons after transplantation into rat sciatic Nerve.
- Oculodentodigital dysplasia Syndrome associated with abnormal cerebral white matter.
- Different cellular and molecular mechanisms for early and late-onset myelin protein zero mutations.
- Gtx, an oligodendrocyte-specific homeodomain protein, has repressor activity.
- Differential distribution of neuregulin in human Brain and spinal fluid.
- Regulation of oleoyl-CoA synthesis in the peripheral Nervous system: demonstration of a link with myelin synthesis.
- Crystal structure of the extracellular domain of human myelin protein zero.
- Axons modulate the expression of proteolipid protein in the CNS.
- Toward a transgenic mouse model of remyelination.
- Nk6, a novel Drosophila homeobox gene regulated by vnd.
- Structure and expression of proteolipid protein in the peripheral Nervous system.
- Appearance of PLP mRNA in specific regions of the developing rat lumbosacral Spinal cord as revealed by in situ hybridization.
- Evidence that the homeodomain protein Gtx is involved in the regulation of oligodendrocyte myelination.
- Complicated hereditary spastic paraparesis with Cerebral white matter lesions.
- Protein zero is necessary for E-cadherin-mediated adherens junction formation in Schwann cells.
- Segmental spinal Muscular atrophy and dermatological findings in a patient with chromosome 18q deletion.
- White matter changes associated with deletions of the long arm of chromosome 18 (18q- Syndrome): a dysmyelinating disorder?
- Heterozygous P0 knockout mice develop a Peripheral neuropathy that resembles chronic inflammatory demyelinating polyneuropathy (CIDP).
- Overcoming cellular immunity to prolong adenoviral-mediated gene expression in sciatic Nerve.
- Axon-Schwann cell interactions regulate the expression of c-jun in Schwann cells.
- Myelin protein zero/P0 phosphorylation and function require an adaptor protein linking it to RACK1 and PKC alpha.
- Correlation between weakness and axonal loss in patients with CMT1A.
- Heterogeneous duplications in patients with Pelizaeus-Merzbacher Disease suggest a mechanism of coupled homologous and nonhomologous recombination.
- A molecular basis for hereditary motor and sensory neuropathy Disorders.
- Modulation of cell-mediated immunity prolongs adenovirus-mediated transgene expression in sciatic Nerve.
- Hereditary motor and sensory neuropathies: a biological perspective.
- Additional copies of the proteolipid protein gene causing Pelizaeus-Merzbacher Disease arise by separate integration into the X chromosome.
- The absence of myelin P0 protein produces a novel molecular phenotype in Schwann cells.
- CNS myelin paranodes require Nkx6-2 homeoprotein transcriptional activity for normal structure.
- Late onset Charcot-Marie-Tooth 2 Syndrome caused by two novel mutations in the MPZ gene.
- Elevated expression of messenger RNA for peripheral myelin protein 22 in biopsied peripheral nerves of patients with Charcot-Marie-Tooth Disease type 1A.
- An adenoviral vector can transfer lacZ expression into Schwann cells in culture and in sciatic Nerve.
- Introduction to the Third International Symposium on Charcot-Marie-Tooth Disorders.
- Regulation of myelin-specific gene expression. Relevance to CMT1.
- Mutations in the cytoplasmic domain of P0 reveal a role for PKC-mediated phosphorylation in adhesion and myelination.
- Peripheral neuropathy caused by proteolipid protein gene mutations.
- Evidence for neuroaxonal injury in patients with proteolipid gene mutations.
- Phenotypic clustering in MPZ mutations.
- The molecular pathogenesis of Pelizaeus-Merzbacher Disease.
- Skin biopsies demonstrate MPZ splicing abnormalities in Charcot-Marie-Tooth Neuropathy 1B.
- Absence of P0 leads to the dysregulation of myelin gene expression and myelin morphogenesis.
- Proteolipid protein mRNA stability is regulated by axonal contact in the rodent peripheral Nervous system.
- T118M PMP22 mutation causes partial loss of function and HNPP-like Neuropathy.
- Proteolipid protein is necessary in Peripheral as well as central myelin.
- Schwann cell expression of PLP1 but not DM20 is necessary to prevent Neuropathy.
- Charcot-Marie-Tooth Disease type 1: molecular pathogenesis to gene therapy.
- Neurological dysfunction and axonal degeneration in Charcot-Marie-Tooth Disease type 1A.
- Patients lacking the major CNS myelin protein, proteolipid protein 1, develop length-dependent axonal degeneration in the absence of demyelination and inflammation.
- Regulation of myelin development.
- A prospective, open-label treatment trial to compare the effect of IFNbeta-1a (Avonex), IFNbeta-1b (Betaseron), and glatiramer acetate (Copaxone) on the relapse rate i...
- Effect of monthly intravenous cyclophosphamide in rapidly deteriorating Multiple sclerosis patients resistant to conventional therapy.
- A prospective, open-label treatment trial to compare the effect of IFN beta-1a (Avonex), IFNbeta-1b (Betaseron), and glatiramer acetate (Copaxone) on the relapse rate ...
Schools
University Of Pennsylvania School Of Medicine
Procedures Preformed
- EMG (Electromyography)
Conditions Treated
- Ataxia
- Autonomic Disorders
- Bell's Palsy
- Brain and Nervous System Cancer (incl. Gliomas, Astrocytoma, Schwannoma, Medulloblastoma, Chordoma)
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Doctors Specialties
- Neurology
Accepted Insurances
Education
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University of Pennsylvania Health System -
Perelman School of Medicine at the University of Pennsylvania
Hospital
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DMC - Detroit Receiving Hospital -
DMC Harper University Hospital
Drug Facts
| NPI NUMBER | 1962440032 | |
| NPPES Provider LastName | KAMHOLZ | |
| NPPES Provider FirstName | JOHN | |
| NPPES Provider ZIPCode | 482012153 | |
| NPPES Provider State | MI | |
| Specialty Description | Neurology | |
| Total Claim Count | 1357.0 | |
| Distinct Opioid Count | 5.0 | |
| Opioid Claim Count | 243.0 | |
| Percent Opioid Claims | 17.91 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1962440032 |
| Last Name Of The Provider | KAMHOLZ |
| First Name Of The Provider | JOHN |
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