ELF3 (1q32.1) (E74 Like ETS Transcription Factor 3)
https://www.genecards.org/cgi-bin/carddisp.pl?gene=ELF3&keywords=ELF3
Enables DNA-binding transcription activator
activity, RNA polymerase II-specific and sequence-specific
double-stranded DNA binding activity. Involved in inflammatory response;
negative regulation of transcription, DNA-templated; and positive
regulation of transcription by RNA polymerase II. Located in Golgi
apparatus; cytosol; and nucleoplasm. [provided by Alliance of Genome
Resources, Apr 2022] GeneCards Summary for ELF3 Gene: ELF3 (E74 Like ETS Transcription Factor 3) is a Protein Coding gene.
Diseases associated with ELF3 include Ampulla Of Vater Cancer and Bladder Urothelial Carcinoma.
Among its related pathways are Pre-NOTCH Expression and Processing and Signal Transduction.
Gene Ontology (GO) annotations related to this gene include DNA-binding transcription factor activity and transcription coactivator activity.
An important paralog of this gene is EHF. UniProtKB/Swiss-Prot Summary for ELF3 Gene: Transcriptional activator that binds and transactivates ETS sequences
containing the consensus nucleotide core sequence GGA[AT]. Acts
synergistically with POU2F3 to transactivate the SPRR2A promoter and
with RUNX1 to transactivate the ANGPT1 promoter. Also transactivates
collagenase, CCL20, CLND7, FLG, KRT8, NOS2, PTGS2, SPRR2B, TGFBR2 and
TGM3 promoters. Represses KRT4 promoter activity. Involved in mediating
vascular inflammation. May play an important role in epithelial cell
differentiation and tumorigenesis. May be a critical downstream effector
of the ERBB2 signaling pathway. May be associated with mammary gland
development and involution. Plays an important role in the regulation of
transcription with TATA-less promoters in preimplantation embryos,
which is essential in preimplantation development (By similarity).
(
ELF3_HUMAN,P78545 ).
Protein attributes for ELF3 Gene Size:371 amino acids
Quaternary structure:
Interacts with TBP. Interacts with CREBBP and EP300; these act as transcriptional coactivators of ELF3 and positively modulate its function. Interacts
with XRCC5/KU86 and XRCC6/KU70; these inhibit the ability of ELF3 to
bind DNA and negatively modulate its transcriptional activity. Associated with CLND7 and POU2F3. Interacts with ZNF768 (PubMed:30476274).
2024 article: (Impact to platin uptake also )
The
copper transporter, SLC31A1, transcriptionally activated by ELF3,
imbalances copper homeostasis to exacerbate cisplatin-induced acute
kidney injury through mitochondrial dysfunction.
Qiu Z, Liu Q, Wang L, Xiong Y, Wu J, Wang M, Yan X, Deng H.
Chem Biol Interact. 2024 Mar 8:110943. doi: 10.1016/j.cbi.2024.110943. Online ahead of print.
PMID: 38462
Acute kidney injury (AKI) is a common complication of cisplatin
chemotherapy, which greatly limits its clinical effect and application.
This study explored the function of solute Carrier Family 31 Member 1
(SLC31A1) in cisplatin-induced AKI and its possible mechanism. Mice and
HK-2 cells were exposed to cisplatin to establish the in vivo and in
vitro AKI models. Cell viability was detected by CCK-8. Mitochondrial
and oxidative damage was determined by Mito-Tracker Green staining,
mtROS level, ATP production, mitochondrial membrane potential, MDA
content and CAT activity. AKI was evaluated by renal function and
histopathological changes. Apoptosis was detected by TUNEL and caspase-3
expression. Molecule expression was measured by RT-qPCR, Western
blotting, and immunohistochemistry. Molecular mechanism was studied by
luciferase reporter assay and ChIP. SLC31A1 level was predominantly
increased by cisplatin exposure in AKI models. Notably, copper ion (Cu+) level was enhanced by cisplatin challenge. Moreover, Cu+
supplementation intensified cisplatin-induced cell death, mitochondrial
dysfunction, and oxidative stress in HK-2 cells, indicating the
involvement of cuproptosis in cisplatin-induced AKI, whereas these
changes were partially counteracted by SLC31A1 knockdown. E74 like ETS
transcription factor 3 (ELF3) could directly bind to SLC31A1 promoter
and promote its transcription. ELF3 was up-regulated and positively
correlated with SLC31A1 expression upon cisplatin-induced AKI. SLC31A1
silencing restored renal function, alleviated mitochondrial dysfunction,
and apoptosis in cisplatin-induced AKI mice. ELF3 transcriptionally
activated SLC31A1 to trigger cuproptosis that drove cisplatin-induced
AKI through mitochondrial dysfunction, indicating that SLC31A1 might be a
promising therapeutic target to mitigate AKI during cisplatin
chemotherapy.
Kuparinkuljettajan funktio:
SLC31A (9q32)
- GeneCards Symbol:
SLC31A1
2
-
Solute Carrier Family 31 Member 1
2
3
4
5
-
CTR1
2
3
4
5
-
HCTR1
2
4
5
-
COPT1
3
4
5
-
Solute Carrier Family 31 (Copper Transporter), Member 1
2
3
-
High Affinity Copper Uptake Protein 1
3
4
-
Copper Transporter 1
3
4
-
Solute Carrier Family 31 (Copper Transporters), Member 1
3
-
Copper Transport 1 Homolog
3
-
NSCT
3
[Truncated CTR1 form]: Mobilizes copper(1+) out of the endosomal
compartment, making copper(1+) available for export out of the cells.
(
COPT1_HUMAN,O15431 )
https://pubmed.ncbi.nlm.nih.gov/35027734/
Does not function as a copper(1+) importer in vivo (By similarity).
However, in vitro functions as low-affinity copper(1+) importer (PubMed:
17944601,
17617060).
Regulator of SLC31A1 which facilitates the cleavage of the SLC31A1 ecto-domain or which stabilizes the truncated form of SLC31A1 (Truncated CTR1
form), thereby drives the SLC31A1 truncated form-dependent endosomal copper export and modulates the copper and cisplatin accumulation via SLC31A1 (By similarity).
(
COPT2_HUMAN,O15432 )
- Ravinnon kupari: Kuparipitoiset ravinteet: Copper sources in food:These has also high Kalium many of them.
Oysters and other shellfish , whole grains, beans, nuts, potatoes, and organ meats (kidneys, liver)
are good sources of copper. Dark leafy greens, dried fruits such as
prunes, cocoa, black pepper, and yeast are also sources of copper in the
diet.
( Nämä kuparinkuljettajat osallistunevat myös platinan kuljetukseen kuten hopeankin).
