Teepu Siddique
| Teepu Siddique | |
|---|---|
| Born | |
| 🏫 Education | Dow Medical College (MBBS, 1973) |
| 💼 Occupation | |
| Known for | Discovery of SOD1, alsin and UBQLN2 mutations in amyotrophic lateral sclerosis |
| 🏅 Awards | Forbes Norris Award (1995) Sheila Essey Award (1996) |
Teepu Siddique is a Pakistani-American neurologist who researches the genetics of amyotrophic lateral sclerosis (ALS). Groups he led or co-led identified mutations in SOD1 (1993), ALS2 (2001) and UBQLN2 (2011) as causes of familial ALS.[1] He is a professor of neurology at Northwestern University's Feinberg School of Medicine in Chicago.
Early life and education
Siddique studied botany at Islamia College, Lahore, affiliated with the University of the Punjab, and received his medical degree from Dow Medical College in Karachi in 1973.[1] In the United States he completed an internship at Perth Amboy General Hospital in New Jersey in 1976 and a residency in neurology at the University of Medicine and Dentistry of New Jersey in 1979.[1] He then held fellowships at the Hospital for Special Surgery in New York City and the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland.[1]
Career
Before Northwestern, Siddique worked at Duke University, where he took part in early genetic linkage studies of familial ALS.[citation needed] In 1991 he joined Northwestern University as a professor in the departments of neurology and cell and molecular biology.[1] At Northwestern he founded the Neuromuscular Program, the Neurogenetics Laboratory and a multidisciplinary ALS clinic.[1][2]
Research
SOD1
In 1993 Siddique was part of the international consortium, with Robert H. Brown Jr. and others, that reported mutations in the gene for copper/zinc superoxide dismutase (SOD1) in families with inherited ALS. It was the first gene found to cause ALS.[3] In 1994 his laboratory, with collaborators, produced the first transgenic mouse model of ALS, which carried a mutant human SOD1 gene.[4]
Alsin
In 2001 his group identified mutations in ALS2, which encodes the protein alsin, as a cause of a juvenile-onset recessive form of ALS.[5]
Ubiquilin 2
In 2011 a team led by Siddique and Han-Xiang Deng reported that mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS with dementia. The study found ubiquilin 2 inclusions in spinal cord and brain tissue from people with familial and sporadic ALS, and the authors proposed that defective protein degradation is common to different forms of the disease.[6]
Awards and honours
- 1995 – Forbes Norris Award, International Alliance of ALS/MND Associations[1]
- 1996 – Sheila Essey Award, American Academy of Neurology (shared with Robert H. Brown Jr.)[1]
- Listed in The Muslim 500[7]
- Hall of Fame, Dow Graduates Association of North America[8]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 "Teepu Siddique". Encyclopedia Britannica. Retrieved 5 October 2026.
- ↑ "Neurodegenerative disease research gift". Northwestern University Feinberg School of Medicine. 2021. Retrieved 5 October 2026.
- ↑ Rosen, D. R.; Siddique, T.; et al. (1993). "Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis". Nature. 362 (6415): 59–62. doi:10.1038/362059a0. PMID 8446170.
- ↑ Gurney, M. E.; et al. (1994). "Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation". Science. 264 (5166): 1772–1775. doi:10.1126/science.8209258. PMID 8209258.
- ↑ Yang, Y.; et al. (2001). "The gene encoding alsin, a protein with three guanine-nucleotide exchange factor domains, is mutated in a form of recessive amyotrophic lateral sclerosis". Nature Genetics. 29 (2): 160–165. doi:10.1038/ng1001-160. PMID 11586297.
- ↑ Deng, H. X.; Chen, W.; et al. (2011). "Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia". Nature. 477 (7363): 211–215. doi:10.1038/nature10353. PMID 21857683.
- ↑ "Prof. Teepu Siddique". The Muslim 500. Retrieved 5 October 2026.
- ↑ "Hall of Fame". DOGANA. Retrieved 5 October 2026.
External links
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