"Tumor Protein p73" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A homolog of p53 TUMOR SUPPRESSOR PROTEIN that encodes full-length trans-activating and N-terminally-truncated (DeltaN) isoforms. Detection of splice variants and isoforms in the nervous system (human TELENCEPHALON, CHOROID PLEXUS; CEREBROSPINAL FLUID), embryonic tissue, human BREAST CANCER; OVARIAN CANCER, suggest roles in cellular differentiation.
| Descriptor ID |
D000072160
|
| MeSH Number(s) |
D12.776.260.885 D12.776.624.776.820 D12.776.660.912 D12.776.930.969
|
| Concept/Terms |
Tumor Protein p73- Tumor Protein p73
- Protein p73, Tumor
- p73, Tumor Protein
- Protein p73
- p73, Protein
- p73 Protein
- Protein, p73
- Tumor Suppressor Protein p73
- Tap73 Protein, Human
- Human Tap73 Protein
- Protein, Human Tap73
|
Below are MeSH descriptors whose meaning is more general than "Tumor Protein p73".
Below are MeSH descriptors whose meaning is more specific than "Tumor Protein p73".
This graph shows the total number of publications written about "Tumor Protein p73" by people in this website by year, and whether "Tumor Protein p73" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 2001 | 0 | 1 | 1 |
| 2004 | 0 | 4 | 4 |
| 2006 | 0 | 1 | 1 |
| 2007 | 0 | 1 | 1 |
| 2008 | 0 | 2 | 2 |
| 2011 | 0 | 2 | 2 |
| 2014 | 0 | 1 | 1 |
| 2016 | 2 | 0 | 2 |
| 2017 | 0 | 2 | 2 |
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Below are the most recent publications written about "Tumor Protein p73" by people in Profiles.
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p73 regulates epidermal wound healing and induced keratinocyte programming. PLoS One. 2019; 14(6):e0218458.
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Do some epithelial ovarian cancers originate from a fallopian tube ciliate cell lineage? Med Hypotheses. 2017 Sep; 107:16-21.
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The p53 family members have distinct roles during mammalian embryonic development. Cell Death Differ. 2017 04; 24(4):575-579.
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De novo missense variants in HECW2 are associated with neurodevelopmental delay and hypotonia. J Med Genet. 2017 02; 54(2):84-86.
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De novo missense variants in HECW2 are associated with neurodevelopmental delay and hypotonia. J Med Genet. 2017 02; 54(2):84-86.
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Novel therapeutic interventions for p53-altered tumors through manipulation of its family members, p63 and p73. Cell Cycle. 2016; 15(2):164-71.
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p53 Activity Dominates That of p73 upon Mdm4 Loss in Development and Tumorigenesis. Mol Cancer Res. 2016 Jan; 14(1):56-65.
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Mdm2 overexpression and p73 loss exacerbate genomic instability and dampen apoptosis, resulting in B-cell lymphoma. Oncogene. 2016 Jan 21; 35(3):358-65.
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IAPP-driven metabolic reprogramming induces regression of p53-deficient tumours in vivo. Nature. 2015 Jan 29; 517(7536):626-30.
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The histone deacetylase inhibitor SAHA sensitizes acute myeloid leukemia cells to a combination of nucleoside analogs and the DNA-alkylating agent busulfan. Leuk Lymphoma. 2014 Jul; 55(7):1625-34.