Molecule Information

General Information of the Molecule (ID: Mol04169)

• Name: Tripartite motif containing 44 (TRIM44) ,Homo sapiens
• Synonyms: Protein DIPB
• Molecule Type: Protein
• Gene Name: TRIM44
• Gene ID: 54765
• Location: chr11:35662775-35818007[+]
• Sequence:
  MASGVGAAFEELPHDGTCDECEPDEAPGAEEVCRECGFCYCRRHAEAHRQKFLSHHLAEY
  VHGSQAWTPPADGEGAGKEEAEVKVEQEREIESEAGEESESEEESESEEESETEEESEDE
  SDEESEEDSEEEMEDEQESEAEEDNQEEGESEAEGETEAESEFDPEIEMEAERVAKRKCP
  DHGLDLSTYCQEDRQLICVLCPVIGAHQGHQLSTLDEAFEELRSKDSGGLKAAMIELVER
  LKFKSSDPKVTRDQMKMFIQQEFKKVQKVIADEEQKALHLVDIQEAMATAHVTEILADIQ
  SHMDRLMTQMAQAKEQLDTSNESAEPKAEGDEEGPSGASEEEDT
• Function: May play a role in the process of differentiation and maturation of neuronal cells (By similarity). May regulate the activity of TRIM17. Is a negative regulator of PAX6 expression (PubMed:26394807). .
• Uniprot ID: TRI44_HUMAN
• Ensembl ID: ENSG00000166326
• HGNC ID: HGNC:19016

Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens

Type(s) of Resistant Mechanism of This Molecule

  MRAP: Metabolic Reprogramming via Altered Pathways

Drug Resistance Data Categorized by Drug

Approved Drug(s) 1 drug(s) in total

Bortezomib

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Metabolic Reprogramming via Altered Pathways (MRAP)

Disease Class: Multiple myeloma [ICD-11: 2A83.0] [1]

• Metabolic Type: Redox metabolism
• Resistant Disease: Multiple myeloma [ICD-11: 2A83.0]
• Resistant Drug: Bortezomib
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: Hela cells; Cervix uteri; Homo sapiens (Human); CVCL_0030
• In Vitro Model: RPMI cells; Blood; Homo sapiens (Human); N.A.
• In Vitro Model: U266 cells; Bone marrow; Homo sapiens (Human); CVCL_0566
• Experiment for Molecule Alteration: Western blot analysis
• Experiment for Drug Resistance: Apoptosis assay
• Mechanism Description: This analysis further identified high TRIM44 expression as predictive of lower responsiveness to proteasome inhibitor (PI) treatments, underscoring its critical function in the unfolded protein response (UPR) in TRIM44-high MM cells. Our findings also demonstrate that TRIM44 facilitates SQSTM1 oligomerization under oxidative stress, essential for its phosphorylation and subsequent autophagic degradation. This process supports the survival of PI-resistant MM cells by activating the NRF2 pathway, which is crucial for oxidative stress response and, potentially, other chemotherapy-induced stressors. Additionally, TRIM44 counters the TRIM21-mediated suppression of the antioxidant response, enhancing MM cell survival under oxidative stress.

References

• Ref 1: TRIM44, a Novel Prognostic Marker, Supports the Survival of Proteasome-Resistant Multiple Myeloma Cells. Cells. 2024 Aug 26;13(17):1431.