DSP
DSP (Desmoplakin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Nasopharyngeal carcinoma.
Overview
A component of desmosome cell-cell junctions which are required for positive regulation of cellular adhesion. Critical for cell-cell adhesion in early stage blastocysts and progression through proamniotic cavity formation. Not required for preimplantation morphogenic process in blastocysts.
IntOGen calls it a driver in 1 cohort (0 activating, 1 loss-of-function), covering Nasopharyngeal Carcinoma.
- Target · the protein and the cell it sits on
- Drug · antibody, small molecule, cell or radioligand
- Effect · signal, damage or kill
In plain words · DSP (Desmoplakin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Nasopharyngeal carcinoma.
- 1 · What it is
DSP (Desmoplakin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Nasopharyngeal carcinoma.
- 2 · What goes wrong in cancer
A component of desmosome cell-cell junctions which are required for positive regulation of cellular adhesion. Critical for cell-cell adhesion in early stage blastocysts and progression through proamniotic cavity formation.
- 3 · How drugs use it
No product in this corpus aims at DSP yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
External identifiers
Sources: HGNC HGNC:3052 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P15924 (protein name, function text, keywords and locations (REST API)); IntOGen DSP (driver in 1 cohort (Act 0, LoF 1); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Biology
A component of desmosome cell-cell junctions which are required for positive regulation of cellular adhesion. Critical for cell-cell adhesion in early stage blastocysts and progression through proamniotic cavity formation. Not required for preimplantation morphogenic process in blastocysts. Required for keratin filament anchoring at the desmosome junction and subsequent organisation of the keratin intermediate filament network within the cytoplasm. Required for anchoring of desmosomes to the microtubule architecture, via its interaction with NIN. Promotes microtubule-mediated GJA1/CX43 trafficking to cell membranes via its interaction with MAPRE1/EB1, thereby facilitating gap junction intracellular communication. Location: Cell projection, axon; Cell junction, desmosome; Cell membrane; Cytoplasm (UniProt). Locus 6p24.3 (HGNC).
- Nasopharyngeal carcinoma: IntOGen driver in 1 cohort (NPC)
Notes
top- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it a loss-of-function (LoF) driver in 1 cohort. Evidence tier "cohort-driver" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
Latest papers
topQuery for this target: (TITLE:"DSP" OR ABSTRACT:"DSP" OR TITLE:"desmoplakin" OR ABSTRACT:"desmoplakin" OR TITLE:"Desmoplakin" OR ABSTRACT:"Desmoplakin" OR TITLE:"KPPS2" OR ABSTRACT:"KPPS2" OR TITLE:"PPKS2" OR ABSTRACT:"PPKS2") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about DSP, not a curated reading list.
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