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Last update 08 May 2025

TSG101

Last update 08 May 2025

Basic Info

Synonyms

ESCRT-I complex subunit TSG101, TSG10, TSG101

+ [5]

Introduction

Component of the ESCRT-I complex, a regulator of vesicular trafficking process. Binds to ubiquitinated cargo proteins and is required for the sorting of endocytic ubiquitinated cargos into multivesicular bodies (MVBs). Mediates the association between the ESCRT-0 and ESCRT-I complex. Required for completion of cytokinesis; the function requires CEP55. May be involved in cell growth and differentiation. Acts as a negative growth regulator. Involved in the budding of many viruses through an interaction with viral proteins that contain a late-budding motif P-[ST]-A-P. This interaction is essential for viral particle budding of numerous retroviruses. Required for the exosomal release of SDCBP, CD63 and syndecan (PubMed:22660413). It may also play a role in the extracellular release of microvesicles that differ from the exosomes (PubMed:22315426).

Drugs associated with TSG101

FGI-1011A6

Target

TSG101

Mechanism

TSG101 inhibitors

Active Org.-

Originator Org.

Gradalis, Inc.

Active Indication-

Inactive Indication

Influenza, Human [+2]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

FGI-102 series

Target

TSG101

Mechanism

TSG101 inhibitors

Active Org.-

Originator Org.

Functional Genetics, Inc.

Active Indication-

Inactive Indication

Virus Diseases

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with TSG101

NCT01299142

/ Unknown statusPhase 1

Phase I Study of Human Monoclonal Antibody (FGI-101-1A6) in Normal Healthy Volunteers

The purpose of this study is to determine the safety and tolerability of the anti-TSG101 human monoclonal antibody (FGI-101-1A6)when administered intravenously to healthy volunteers.

Start Date01 Jan 2011

Sponsor / Collaborator

Functional Genetics, Inc.

[+1]

100 Clinical Results associated with TSG101

100 Translational Medicine associated with TSG101

0 Patents (Medical) associated with TSG101

1,025

Literatures (Medical) associated with TSG101

01 Oct 2025·Biomaterials

Therapeutic potential of urinary extracellular vesicles in delivering functional proteins and modulating gene expression for genetic kidney disease

Article

Author: Khan, Taranatee ; Dudaney, Megan ; Hallows, Kenneth R ; Pastor-Soler, Nuria M ; Osouli, Ali ; Huang, Yi ; Chaudhuri, Baishali ; Pham, Jessica ; Mancino, Valeria ; Li, Hui ; Chung, Eun Ji

Chronic kidney disease (CKD) is a widespread health concern, impacting approximately 600 million individuals worldwide and marked by a progressive decline in kidney function. A common form of CKD is autosomal dominant polycystic kidney disease (ADPKD), which is the most inherited genetic kidney disease and affects greater than 12.5 million individuals globally. Given that there are over 400 pathogenic PKD1/PKD2 mutations in patients with ADPKD, relying solely on small molecule drugs targeting a single signaling pathway has not been effective in treating ADPKD. Urinary extracellular vesicles (uEVs) are naturally released by cells from the kidneys and the urinary tract, and uEVs isolated from non-disease sources have been reported to carry functional polycystin-1 (PC1) and polycystin-2 (PC2), the respective products of PKD1 and PKD2 genes that are mutated in ADPKD. uEVs from non-disease sources, as a result, have the potential to provide a direct solution to the root of the disease by delivering functional proteins that are mutated in ADPKD. To test our hypothesis, we first isolated uEVs from healthy mice urine and conducted a comprehensive characterization of uEVs. Then, PC1 levels and EV markers CD63 and TSG101 of uEVs were confirmed via ELISA and Western blot. Following characterization of uEVs, the in vitro cellular uptake, inhibition of cyst growth, and gene rescue ability of uEVs were demonstrated in kidney cells. Next, upon administration of uEVs in vivo, uEVs showed bioavailability and accumulation in the kidneys. Lastly, uEV treatment in ADPKD mice (Pkd1^fl/fl;Pax8-rtTA;Tet-O-Cre) showed smaller kidney size, lower cyst index, and enhanced PC1 levels without affecting safety despite repeated treatment. In summary, we demonstrate the potential of uEVs as natural nanoparticles to deliver protein and gene therapies for the treatment of chronic and genetic kidney diseases such as ADPKD.

02 Jun 2025·Journal of Cell Biology

ESCRT-I and PTPN23 mediate microautophagy of ubiquitylated tau aggregates

Article

Author: Hirayama, Shoshiro ; Sato, Yusuke ; Sakurai, Yasuyuki ; Murata, Shigeo ; Lo, Megan ; Shibata, Yuri ; Ao, Shinpei ; Men, Yusen

Protein aggregates are degraded by both the autophagy–lysosomal and the ubiquitin–proteasome pathways. Macroautophagy and microautophagy, two forms of the autophagy–lysosomal pathway, are widely conserved across eukaryotes. While macroautophagy has been extensively studied in the context of degradation of protein aggregates, microautophagy remains less explored. Here, we identify the UBAP1-containing ESCRT-I complex and PTPN23 as new regulators for degradation of aggregated proteins through an unbiased genome-wide CRISPR knockout screen, using a cell line expressing tau repeat domain (tauRD) aggregates. ESCRT-I recognizes ubiquitylated tauRD via the UEV domain of TSG101. The accessory protein PTPN23, instead of ESCRT-II, bridges ESCRT-I and ESCRT-III to complete the endosomal microautophagy of ubiquitylated tauRD aggregates. Our results uncover the molecular mechanism underlying the degradation of tau aggregates by endosomal microautophagy.

01 Jun 2025·Journal of Molecular Biology

High Risk, High Reward: By Selecting Tsg101, A Protein That Sorts The Trash, As Our Personal ESCRT, Both HIV And I Were Able To Bud

Review

Author: Carter, Carol A

Being asked to write this "Reflections"-type article is a special honor offered at the end of one's career and I am grateful for the opportunity to think back over the more than 4-decade span of my career in the field of HIV/AIDS Retrovirology. Although at this point in time there is still no vaccine or curative therapy for HIV/AIDS, this invitation to reminiscence comes in the year of FDA approval of Lenacapavir, the first-in-class anti-HIV agent targeting the viral capsid. This triumph in the field is the culmination of efforts of many, including some in my own laboratory, who were among the first to produce recombinant capsid protein (CAp24) for structural and biochemical studies. A current drawback of this drug is its low genetic barrier to viral resistance. The research finding considered to be our most important contribution to the field of HIV research was framed by the challenge to suppress the emergence of resistant variants, and I describe the paths that drove me to risk exploration of the non-traditional for potential solutions. Finally, I share my views on what I consider to be an important open question for the future: how to achieve greater diversity and inclusion in Science.

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TSG101

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