Associate Professor, Medicine, University of Maryland School of Medicine
Nephrology
Dr. Terry Watnick, MD
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Terry Watnick is an expert in the field of Nephrology. She went to medical school at Yale University School of Medicine. Yale University School of Medicine is one of the top medical schools in the US. Yale University School of Medicine is ranked 7/57 in Research/PrimaryCare. She received 1 awards: "CMS Meaningful Use Stage 1 Certification". Doctor Terry Watnick, MD is a published doctor and has 40 publications published. The lastest was: 'Somatic mutation in individual liver cysts supports a two-hit model of cystogenesis in autosomal dominant polycystic kidney disease.' Terry Watnick accepts Medicare payments and is registered with Medicare.gov.
Publications
- Vascular complications in autosomal dominant polycystic kidney disease.
- Novel inhibitors of nuclear transport cause cell cycle arrest and decrease cyst growth in ADPKD associated with decreased CDK4 levels.
- Polycystin signaling is required for directed endothelial cell migration and lymphatic development.
- A Pkd1-Fbn1 Genetic Interaction Implicates TGF-β Signaling in the Pathogenesis of Vascular Complications in Autosomal Dominant Polycystic Kidney Disease.
- Polycystic kidney disease: Polycystin-1 and polycystin-2-it's complicated.
- Ciliary membrane proteins traffic through the Golgi via a Rabep1/GGA1/Arl3-dependent mechanism.
- Molecular basis of autosomal dominant polycystic kidney disease.
- Somatic PKD2 mutations in individual kidney and liver cysts support a "two-hit" model of cystogenesis in type 2 autosomal dominant polycystic kidney disease.
- Mutations of PKD1 in ADPKD2 cysts suggest a pathogenic effect of trans-heterozygous mutations.
- Mutation detection of PKD1 identifies a novel mutation common to three families with aneurysms and/or very-early-onset disease.
- Bilineal disease and trans-heterozygotes in autosomal dominant polycystic kidney disease.
- Thirteen novel mutations of the replicated region of PKD1 in an Asian population.
- Aberrant splicing in the PKD2 gene as a cause of polycystic kidney disease.
- Somatic mutation as mechanism for cyst formation in autosomal dominant polycystic kidney disease.
- Somatic mutation in individual liver cysts supports a two-hit model of cystogenesis in autosomal dominant polycystic kidney disease.
- Gene conversion is a likely cause of mutation in PKD1.
- An unusual pattern of mutation in the duplicated portion of PKD1 is revealed by use of a novel strategy for mutation detection.
- Polycystin: in vitro synthesis, in vivo tissue expression, and subcellular localization identifies a large membrane-associated protein.
- The molecular basis of focal cyst formation in human autosomal dominant polycystic kidney disease type I.
- Microalbuminuria and hypertension in long-term renal donors.
- A missense mutation in PKD1 attenuates the severity of renal disease.
- Tolvaptan in autosomal dominant polycystic kidney disease: three years'' experience.
- Drosophila sperm swim backwards in the female reproductive tract and are activated via TRPP2 ion channels.
- Polycystin-1 regulates STAT activity by a dual mechanism.
- Pkd1 and Pkd2 are required for normal placental development.
- Not all renal cysts are created equal.
- mTOR inhibitors in polycystic kidney disease.
- Aortic abnormalities in males with Alport syndrome.
- Diagnosis and screening of autosomal dominant polycystic kidney disease.
- DNA testing for live kidney donors at risk for autosomal dominant polycystic kidney disease.
- The tuberous sclerosis proteins regulate formation of the primary cilium via a rapamycin-insensitive and polycystin 1-independent pathway.
- TRPP2 and TRPV4 form a polymodal sensory channel complex.
- Loss of Bardet Biedl syndrome proteins causes defects in peripheral sensory innervation and function.
- Genetic interaction studies link autosomal dominant and recessive polycystic kidney disease in a common pathway.
- Evaluating the clinical utility of a molecular genetic test for polycystic kidney disease.
- A flagellar polycystin-2 homolog required for male fertility in Drosophila.
- From cilia to cyst.
- Cleavage of polycystin-1 requires the receptor for egg jelly domain and is disrupted by human autosomal-dominant polycystic kidney disease 1-associated mutations.
- Mutation analysis of the entire replicated portion of PKD1 using genomic DNA samples.
Schools
Yale University
Yale University School Of Med
Johns Hopkins University
Doctors Specialties
- Internal Medicine
- Nephrology
Accepted Insurances
Awards
- CMS Meaningful Use Stage 1 Certification
Education
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Johns Hopkins University -
Yale-New Haven Hospital -
Yale University School of Medicine
Hospital
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University of Maryland Medical Center
Drug Facts
| NPI NUMBER | 1275579989 | |
| NPPES Provider LastName | WATNICK | |
| NPPES Provider FirstName | TERRY | |
| NPPES Provider ZIPCode | 212011544 | |
| NPPES Provider State | MD | |
| Specialty Description | Internal Medicine | |
| Total Claim Count | 50.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1275579989 |
| Last Name Of The Provider | WATNICK |
| First Name Of The Provider | TERRY |
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