Because of its key role in secondary phenylpropanoid metabolism, Phe ammonia-lyase is one of the most extensively studied plant enzymes. To provide a basis for detailed structure–function studies, the enzyme from parsley (Petroselinum crispum) was crystallized, and the structure was elucidated at 1.7-Å resolution. It contains the unusual electrophilic 4-methylidene-imidazole-5-one group, which is derived from a tripeptide segment in two autocatalytic dehydration reactions. The enzyme resembles His ammonia-lyase from the general His degradation pathway but contains 207 additional residues, mainly in an N-terminal extension rigidifying a domain interface and in an inserted α-helical domain restricting the access to the active center. Presumably, Phe ammonia-lyase developed from His ammonia-lyase when fungi and plants diverged from the other kingdoms. A pathway of the catalyzed reaction is proposed in agreement with established biochemical data. The inactivation of the enzyme by a nucleophile is described in detail

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The structures of beta-methylenethiazole-4-carboxamide adenine dinucleotide (TAD), NAD(+), and NADH as bound to ecto-ADP-ribosyltransferase 2.2 from rat and to its mutants E189I and E189A, respectively, have been established. The positions and conformations of NAD(+) and its analogues agree in general with those in other ADP-ribosyltransferases. The kinetic constants for NAD(+) hydrolysis were determined by RP-HPLC. The specific activity amounts to 26 units/mg, which is 6000-fold higher than a previously reported rate and 500-fold higher than the hydrolysis rates of other ADP-ribosyltransferases, confirming that hydrolysis is the major function of this enzyme. On the basis of structures and mutant activities, a catalytic mechanism is proposed. The known auto-ADP-ribosylation of the enzyme at the suggested position R184 is supported by one of the crystal structures where the nucleophile position is occupied by an Neta atom of this arginine which in turn is backed up by the base E159.

ODERN concepts of cancer immunology originated from the classic observations by Jensen, Loeb, Tyzzer, and Little in the early years of the 20th century of the rejection of transplanted allogeneic tumors and the acceptance of syngeneic tumors. 1 Despite this law of transplantation, there are several clinical examples of the accidental transplantation of a malignant tumor or tumor cells into a healthy recipient. [2][3][4][5] We describe the accidental transplantation of a malignant sarcoma from a patient to a surgeon. Using molecular methods, we showed that the sarcomas in the unrelated patient and surgeon were genetically identical. CASE REPORTA 32-year-old man underwent emergency surgery to remove a malignant fibrous histiocytoma from his abdomen and died shortly thereafter of postoperative complications. During the operation the 53-year-old surgeon injured the palm of his left hand while placing a drain. The lesion was immediately disinfected and dressed. Five months later, the surgeon consulted a hand specialist because of a hard, circumscribed, tumor-like swelling, 3.0 cm (1.2 in.) in diameter, in his left palm at the base of the middle finger, where he had been injured during the operation. An extensive examination, including laboratory tests, did not reveal any signs of immune deficiency. The tumor was completely excised. Histologic examination revealed that it was a malignant fibrous histiocytoma. Two years later, the surgeon's condition was good, and there was no evidence of recurrence or metastasis of the tumor.The pathologist who investigated both the patient's tumor and the surgeon's tumor raised the question whether the tumors were identical.