Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.
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Question: Hoping to rebound from their three-game losing streak, the Raiders flew to Dolphin Stadium for a Week 11 duel with the Miami Dolphins. In the first quarter, Oakland trailed early as Dolphins WR Ted Ginn, Jr. got a 40-yard TD run. In the second quarter, the Raiders responded with kicker Sebastian Janikowski getting a 21-yard field goal. In the third quarter, Oakland started to catch up as DE Jay Richardson sacked QB Chad Pennington in his own endzone for a safety. Miami would answer with RB Patrick Cobbs getting a 10-yard TD run. In the fourth quarter, the Raiders took the lead as Janikowski got a 37-yard field goal, along with WR Johnnie Lee Higgins returning a punt 93 yards for a touchdown. However, the Dolphins sealed Oakland's fate as kicker Dan Carpenter nailed a 38-yard field goal.

Answer: Which player scored a safety?


Question: Parkinson's disease is the most common neurodegenerative movement disorder. The motor impairments of Parkinson's disease are caused by the loss of dopaminergic neurons in the substantia nigra and associated with the appearance of fibrillar aggregates of -synuclein (-syn) called Lewy bodies. Approximately 90% of -syn deposited in Lewy bodies is phosphorylated at serine 129 (Ser129). In contrast, only 4% or less of total -syn is phosphorylated at this residue in the normal brain. This suggests that the accumulation of Ser129-phosphorylated -syn leads to the formation of Lewy bodies and dopaminergic neurodegeneration in Parkinson's disease. Our laboratory and others have performed experiments using in vivo models of Parkinson's disease to elucidate the role of increased Ser129 phosphorylation in -syn neurotoxicity. However, there has been a lack of consistency among these models. In this review, we summarize the main findings regarding the relationship between Ser129 phosphorylation and -syn neurotoxicity, and examine the differences among models. We further discuss the role of Ser129 phosphorylation in -syn aggregation and the future directions to test the potential of Ser129 phosphorylation as a therapeutic target for slowing the progression of Parkinson's disease.

Answer: Which residue of alpha-synuclein was found to be phosphorylated in Lewy bodies?


Question: Imatinib mesylate is a new drug that can inhibit the tyrosine kinase activity of Bcr-Abl, the receptors for platelet-derived growth factor receptor(PDGF) and stem cell factor, or c-kit. Chronic myeloid leukemia (CML) is distinguished by the presence of a reciprocal translocation between chromosomes 9 and 22 that results in a shortened chromosome 22, termed the Philadelphia(Ph) chromosome. As a result of the translocation, a fusion gene called the Bcr-Abl gene is created from two normal cellular genes, encoding a chimeric Bcr-Abl protein with a deregulated tyrosine kinase activity. The expression of Bcr-Abl tyrosine kinase has been shown to be necessary and sufficient for the transformed phenotype of CML cells. Imatinib can block the kinase activity of Bcr-Abl, thus inhibiting the proliferation of Ph-positive progenitors, and has shown activity against all phases of CML, though responses are most substantial and durable in patients in the chronic phase. An international phase III study which compared the efficacy of imatinib with that of interferon alpha combined with low-dose cytarabine in newly diagnosed chronic-phase CML showed the rate of major cytogenetic response at 24 months was 90%, including 82% of complete cytogenetic response. These results indicated that imatinib was superior to interferon-containing treatment as a first-line therapy. More than 10,000 patients worldwide, including those in Japan, have been treated with imatinib in clinical trials, and a lot of information has been accumulated on the use of this drug. The aim of this article is to review the use of this drug and the practical management of patients with chronic myeloid leukemia.

Answer:
What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?