Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By using polyacrylamide gel electrophoresis, sera were tested on cancer-associated globulin from female patients bearing gynaecological cancers: 45 cervical, 21 endometrial and 38 ovarian. As a control, normal sera were taken from 97 healthy women. Sera were also taken from patients with benign neoplasias: 59 cervical dysplasias, 72 endometrial fibromyomas and 47 ovarian cystadenomas. The cancer-associated globulin was evaluated, as an antibody to a cancer antigen that consists of ceramide-lactoside conjugated to a protein integrated in a tumor cell membrane. This serum globulin can be shown densitometrically as the fourth post-transferrin peak (PTP 4). It was found in 69% cervical cancer patients, 52% of the endometrial cancer patients and 89% of the ovarian cancer patients. False positive results were detected in 11% of the normal sera and 25% of the sera from patients with benign neoplasias.
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PMID:Cancer-associated serum globulin determined in patients with cervical, endometrial and ovarian cancer. 769 81

To assess the development of inspiratory and expiratory muscle fatigue during normocapnic hyperpnoea, we studied fourteen healthy men performing 8min hyperpnoea, 6min pause, 8min hyperpnoea, etc., until task failure. Twitch transdiaphragmatic (P(di,tw)) and gastric (P(ga,tw)) pressures were measured during cervical and thoracic magnetic nerve stimulation, before hyperpnoea, after every 8min of hyperpnoea, and at task failure (i.e., at 25.3+/-4.7min). P(di,tw) decreased during the first 16min (-28+/-7%, p<0.001) and P(ga,tw) during the first 8min (-20+/-7%, p<0.001) of hyperpnoea without further change until task failure. During inspiration, the pressure-time-product of oesophageal pressure (PTP(oes)) increased relative to PTP(di) during the first 16min (+11+/-21%, p<0.05). Similarly, during expiration, PTP(oes) increased relative to PTP(ga) during the first 8min (+10+/-16%, p<0.05). Also, blood lactate concentration and respiratory sensations significantly increased during the first 8min (+1.0+/-0.5mmoll(-1), p<0.001) and 16min (breathlessness +1.6+/-1.8 points, respiratory effort +5.9+/-2.2points, p<0.001), respectively. We conclude that, during hyperpnoea, contractile fatigue of the diaphragm and abdominal muscles develops long before task failure and may trigger an increased recruitment of rib cage muscles.
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PMID:Development of respiratory muscle contractile fatigue in the course of hyperpnoea. 1880 66

In conclusion, we are starting to uncover important activities of PTPs in breast cancer initiation, progression and maintenance. Studies of SHP2 and PTP1B have exposed them as potentially important targets for the treatment or prevention of breast cancer, not to mention the importance of PTP1B in diabetes. However, the appropriateness of specific inhibitors has to be fully confirmed, especially given the differential involvement of PTPs in an organ-dependent fashion. Crucial issues for future studies include the participation of other PTPs in tissue development and maintenance as well as cancer, and the signaling networks perturbed by PTP inactivation. This approach may lead to the discovery of novel signaling mechanisms regulated by PTPs and a better understanding of cancer-associated pathways.
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PMID:Targeting protein-tyrosine phosphatases in breast cancer. 2262 83

The proto-oncogene PTPN11 encodes a cytoplasmic protein tyrosine phosphatase, SHP2, which is required for normal development and sustained activation of the Ras-MAPK signaling pathway. Germline mutations in SHP2 cause developmental disorders, and somatic mutations have been identified in childhood and adult cancers and drive leukemia in mice. Despite our knowledge of the PTPN11 variations associated with pathology, the structural and functional consequences of many disease-associated mutants remain poorly understood. Here, we combine X-ray crystallography, small-angle X-ray scattering, and biochemistry to elucidate structural and mechanistic features of three cancer-associated SHP2 variants harboring single point mutations within the N-SH2:PTP interdomain autoinhibitory interface. Our findings directly compare the impact of each mutation on autoinhibition of the phosphatase and advance the development of structure-guided and mutation-specific SHP2 therapies.
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PMID:Structural and Functional Consequences of Three Cancer-Associated Mutations of the Oncogenic Phosphatase SHP2. 2703 Feb 75