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Intersectin - many facets of a scaffold protein
Mubashir Mintoo, Vinodh Rajagopalan, John P O'Bryan. Biochemical Society transactions, 2024-02-28
Topic: Disease mechanisms in lab and animal studies
Intersectin (ITSN) is a multi-domain scaffold protein with a diverse array of functions including regulation of endocytosis, vesicle transport, and activation of various signal transduction pathways. There are two ITSN genes located on chromosomes 21 and 2 encoding for proteins ITSN1 and ITSN2, respectively. Each ITSN gene encodes two major isoforms, ITSN-Long (ITSN-L) and ITSN-Short (ITSN-S), due to alternative splicing. ITSN1 and 2, collectively referred to as ITSN, are implicated in many physiological and pathological processes, such as neuronal maintenance, actin cytoskeletal rearrangement, and tumor progression. ITSN is mis-regulated in many tumors, such as breast, lung, neuroblastomas, and gliomas. Altered expression of ITSN is also found in several neurodegenerative diseases, such as Down Syndrome and Alzheimer's disease. This review summarizes recent studies on ITSN and provides an overview of the function of this important family of scaffold proteins in various biological processes.
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APA 7th
Mintoo, M., Rajagopalan, V., & O'Bryan, J. P. (2024). Intersectin - many facets of a scaffold protein. Biochemical Society transactions. https://doi.org/10.1042/bst20211241
Vancouver
Mintoo M, Rajagopalan V, O'Bryan JP. Intersectin - many facets of a scaffold protein. Biochemical Society transactions. 2024. doi:10.1042/bst20211241. PMID: 38174740.
BibTeX
@article{mintoo2024-38174740,
author = {Mintoo, Mubashir and Rajagopalan, Vinodh and O'Bryan, John P},
title = {{Intersectin - many facets of a scaffold protein}},
journal = {Biochemical Society transactions},
year = {2024},
doi = {10.1042/bst20211241},
pmid = {38174740},
url = {https://doi.org/10.1042/bst20211241}
}
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Key findings
- Each ITSN gene encodes two major isoforms, ITSN-Long (ITSN-L) and ITSN-Short (ITSN-S), due to alternative splicing.
- ITSN1 and 2, collectively referred to as ITSN, are implicated in many physiological and pathological processes, such as neuronal maintenance, actin cytoskeletal rearrangement, and tumor progression.
- ITSN is mis-regulated in many tumors, such as breast, lung, neuroblastomas, and gliomas.
- Altered expression of ITSN is also found in several neurodegenerative diseases, such as Down Syndrome and Alzheimer's disease.
- This review summarizes recent studies on ITSN and provides an overview of the function of this important family of scaffold proteins in various biological processes.
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Study details
- Evidence strengthLow
How this study scored 43/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 24 of the 56 points we could judge it on, which is 43 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Biochemical Society transactions) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2024 — within 3 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 38174740) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 24 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 24 of the 56 points we could judge it on is 43 out of 100. |
| Total | 43 / 100 | — |
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