| 1999 |
ANX7/ANXA7 encodes a Ca2+-activated GTPase that supports Ca2+/GTP-dependent secretion events and Ca2+ channel activities; the homozygous knockout (anx7-/-) is embryonically lethal at E10 due to cerebral hemorrhage, while heterozygous anx7(+/-) mice show defective insulin secretion linked to profound reduction in IP3 receptor expression and function in pancreatic islets. |
Gene knockout mouse model (anx7-/- and anx7+/-), electrophysiology, electrooptical Ca2+ recordings, insulin secretion assays |
Proceedings of the National Academy of Sciences of the United States of America |
High |
10570150
|
| 2001 |
Wild-type ANX7 transfection markedly reduces human prostate tumor cell proliferation and colony formation in LNCaP and DU145 cell lines, demonstrating tumor suppressor activity; loss of heterozygosity at the ANX7 locus (10q21) is found in 35% of primary prostate tumors. |
Transfection of wild-type ANX7 into prostate tumor cell lines, colony formation assay, loss-of-heterozygosity analysis with microsatellite markers, tissue microarray immunohistochemistry |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
11287641
|
| 2003 |
Haploinsufficiency of Anx7 in the Anx7(+/-) mouse drives genomic instability, reduction of multiple tumor suppressor genes, DNA repair genes, and apoptosis-related genes, and promotes spontaneous tumorigenesis (23% incidence) with chromosomal aberrations. |
Anx7(+/-) knockout mouse; genome array expression profiling; spectral karyotyping; in situ analysis by tissue imprinting; laser-capture microdissection |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
14608035
|
| 2002 |
In Anx7(+/-) knockout mice, chromaffin cells of the adrenal gland show defective IP3 receptor expression and an inability to discriminate nutritional state (fed vs. fasted), resulting in sustained expression of nutritionally sensitive genes (chromogranin A/B, DβH) and adrenal gland hypertrophy/chromaffin cell hyperplasia. |
Anx7(+/-) knockout mouse; cDNA microarray; adrenal gland phenotypic analysis |
Annals of the New York Academy of Sciences |
Medium |
12438089
|
| 2010 |
A multi-hnRNP complex (containing hnRNP A1, A2/B1, and K) binds the steroid nuclear hormone receptor element cluster at the ANXA7 promoter (-1086/-890) specifically in androgen-resistant prostate cancer cells (PC3), but not in normal prostate cells (PrEC), leading to aberrant ANXA7 transcription and alternative splicing; hnRNPA2/B1 antibody interference validated this regulation. |
Deletion mapping/promoter activity assays; Genomatix analysis; gel-shift (EMSA); MALDI-TOF mass spectrometry identification of hnRNP proteins; antibody interference assay; Ingenuity Pathway Analysis |
Oncogene |
Medium |
20190808
|
| 2012 |
BART binds directly to ANX7 and the BART-ANX7 complex reduces PKCα activity; knockdown of either BART or ANX7 increases PKCα activity and enhances invasiveness of pancreatic cancer cells, which is abrogated by PKCα-specific inhibitors. |
Co-immunoprecipitation (BART-ANX7 interaction); knockdown of BART and ANX7; PKCα activity assay; invasion assay; PKCα inhibitor treatment |
PloS one |
Medium |
22532868
|
| 2012 |
In Anx7(+/-) beta-cells, the muscarinic agonist carbachol and ryanodine receptor agonists (caffeine, 4-chloro-m-cresol) have more potent depolarizing effects and augment glucose-induced insulin secretion; however, ryanodine receptor-mediated Ca2+ mobilization itself is not affected, indicating that the Anx7(+/-) mutation alters downstream signaling pathways associated with IP3 receptors and ryanodine receptors, not the Ca2+ stores directly. |
Anx7(+/-) knockout mouse beta-cells; electrophysiology; intracellular Ca2+ measurements; insulin secretion assay; pharmacological agonists (carbachol, caffeine, 4-chloro-m-cresol) |
Cellular physiology and biochemistry |
Medium |
22613970
|
| 2017 |
Activation of ANXA7 GTPase by small molecule SEC suppresses prostate cancer metastasis by promoting AMPK phosphorylation, leading to decreased mTORC1 activity, suppressed STAT3 nuclear translocation, and downregulation of pro-metastatic genes (CCL2, APLN, IL6ST); RKIP interacts with ANXA7 and impairs SEC-induced GTPase activation and downstream signaling. |
Small molecule (SEC) GTPase activation; AMPK/mTORC1/STAT3 pathway analysis by Western blot; RKIP-ANXA7 interaction; in vivo orthotopic prostate cancer metastasis model |
Cancer letters |
Medium |
29247827
|
| 2016 |
Small molecule ABO directly targets ANXA7 and inhibits its GTPase activity; inhibition of ANXA7 GTPase causes increased TGFB2-OT1 expression, which elevates LARP1, leading to enhanced HMBOX1 translation in vascular endothelial cells; ABO fails to increase HMBOX1 in ANXA7-deficient HUVECs, confirming ANXA7 dependency. |
Small molecule (ABO) GTPase inhibition; ANXA7 knockdown; HMBOX1 protein quantification; TGFB2-OT1/LARP1 expression analysis; in vivo apoE-/- mouse model |
The international journal of biochemistry & cell biology |
Medium |
27506770
|
| 2019 |
Inhibition of ANXA7 GTPase activity by ABO causes ANXA7 to translocate into the nucleus where it interacts with XRN2 (5'→3' exoribonuclease); decreased XRN2 phosphorylation promotes read-through transcription of MROH7-TTC4 lncRNA, which is then processed by TIA1 into MROH7 and TTC4 to inhibit vascular endothelial cell apoptosis. |
GTPase inhibitor (ABO); lncRNA microarray; Co-immunoprecipitation (ANXA7-XRN2); nuclear translocation imaging; TIA1 binding assay |
The FEBS journal |
Medium |
31408583
|
| 2019 |
ANXA7 knockdown inhibits JAK1/STAT3 pathway activation in trophoblast HTR-8/SVneo cells, reduces BCL2 levels, promotes apoptosis, and inhibits proliferation; ANXA7 overexpression has the opposite effect, establishing ANXA7/JAK1/STAT3 as a regulatory pathway in trophoblast survival. |
siRNA knockdown and overexpression in HTR-8/SVneo cells; Western blot; flow cytometry (apoptosis); CCK-8 proliferation assay |
American journal of reproductive immunology |
Medium |
31446642
|
| 2020 |
ANXA7 translocates to impaired mitochondria upon CCCP-induced mitochondrial damage and plays a pivotal role in Parkin-dependent mitophagy by interacting with BASP1. |
Data-independent acquisition quantitative mitochondrial proteomics; mitochondrial fractionation/translocation assay; Co-immunoprecipitation (ANXA7-BASP1); CCCP treatment |
Journal of proteome research |
Medium |
31975592
|
| 2020 |
ANXA7 overexpression promotes proliferation, cell cycle progression, and cell adhesion-mediated drug resistance in multiple myeloma cells through upregulation of CDC5L; co-immunoprecipitation confirmed ANXA7 binds CDC5L, and CDC5L knockdown reverses ANXA7 overexpression effects. |
ANXA7 overexpression and knockdown in U266/RPMI8226 cells; co-immunoprecipitation (ANXA7-CDC5L); proliferation, cell cycle, and apoptosis assays; BMSC co-culture drug resistance model |
Aging |
Medium |
32526706
|
| 2021 |
LEPR interacts with ANXA7 (confirmed by co-immunoprecipitation) and regulates ERK1/2 and JAK2/STAT3 signaling via ANXA7 in hepatocellular carcinoma lymphatic metastatic cells. |
Co-immunoprecipitation (LEPR-ANXA7); western blot for ERK1/2 and JAK2/STAT3; LEPR knockdown/overexpression functional assays |
Cancer cell international |
Low |
33397392
|
| 2023 |
ANXA7 interacts with LAMP5 (lysosomal-associated membrane protein 5) in neurons; the Asp411 mutation of ANXA7 markedly impairs the ANXA7-LAMP5 interaction. Activated ANXA7 GTPase promotes autophagy via the mTOR/TFEB pathway, inhibits neuronal apoptosis after OGD/R, and stabilizes LAMP5 protein expression; LAMP5 overexpression rescues defects caused by ANXA7 downregulation. |
Co-immunoprecipitation (ANXA7-LAMP5); site-directed mutagenesis (Asp411); GTPase activation assay; ANXA7 overexpression lentivirus; CatWalk assay (SCI mice); mTOR/TFEB pathway analysis; autophagy and apoptosis assays |
Cell death discovery |
Medium |
37620352
|
| 2023 |
A dominant-negative triple mutant of ANXA7 (DNTM/DN-ANXA7J) in the GX(X)GT endonexin-fold repeats suppresses membrane fusion with artificial membranes, alters calcium and phospholipid binding, and in prostate cancer cells reduces IP3 receptor expression and modulates PI3K/AKT/mTOR signaling while affecting phosphatidylserine exposure, membrane permeabilization, and apoptosis. |
Site-directed mutagenesis (triple mutant); artificial membrane fusion assay; calcium and phospholipid binding assays; IP3R expression analysis; PI3K/AKT/mTOR pathway Western blot; cell death/apoptosis assays in prostate cancer cells |
International journal of molecular sciences |
Medium |
37240163
|
| 2014 |
Wild-type ANXA7 in LNCaP prostate cancer cells induces G1-arrest and programmed cell death while preserving total FOXO3A expression without hyperphosphorylation (enabling FOXO3A nuclear translocation); ANXA7 tumor suppression operates through a mechanism distinct from p53, which fails to prevent SGK1-mediated FOXO3A phosphorylation and cytoplasmic retention. |
Transfection of wt-ANXA7 vs. p53 in LNCaP cells; cell cycle analysis; apoptosis assays; FOXO3A phosphorylation and localization analysis by Western blot; Ingenuity Pathway Analysis |
BioMed research international |
Low |
24864229
|
| 2018 |
Wild-type ANXA7 abolishes expression of oncogenic low-molecular weight (LMW) cyclin E in hormone-resistant prostate (DU145) and breast cancer cells; a dominant-negative ANXA7 mutant (nMMM-ANXA7, lacking phosphatidylserine liposome aggregation properties) fails to abrogate LMW-cyclin E and simultaneously induces FGF8 in DU145, allowing continued cell cycle progression. |
Adenoviral wt-ANXA7 and dominant-negative nMMM-ANXA7 overexpression; cell cycle analysis; Western blot for LMW-cyclin E and FGF8; comparison across prostate (DU145) and breast (MDA-MB-231, -435) cancer lines |
Trends in cancer research |
Low |
30369774
|
| 2024 |
ZBTB16 interacts with ANXA7 protein (confirmed by co-IP); ZBTB16 promotes ANXA7 expression, which subsequently inhibits Cyclin B1 expression; UHRF1 suppresses ZBTB16 by promoting ZBTB16 promoter methylation via DNMT1 recruitment, thereby reducing ANXA7 and enabling breast cancer cell proliferation. |
Co-immunoprecipitation (ZBTB16-ANXA7); methylation-specific PCR; ChIP assay; UHRF1/ZBTB16/ANXA7 knockdown and overexpression; cell cycle, proliferation, and apoptosis assays; in vivo xenograft |
Acta biochimica et biophysica Sinica |
Medium |
39308302
|
| 2026 |
RNF168 promotes ubiquitination and degradation of ANXA7; loss of ANXA7 suppresses autophagy and induces NLRP3 inflammasome-mediated pyroptosis in intestinal epithelial cells, promoting Crohn's disease progression; ELK1 transcription factor upregulates RNF168 as the upstream regulator. |
Co-immunoprecipitation and mass spectrometry (RNF168-ANXA7 interaction); ubiquitination assay; ANXA7 knockdown/overexpression; autophagy and pyroptosis assays; IL-10 KO and RNF168flox/flox;Villin-Cre mouse models; organoids |
Apoptosis |
Medium |
41518435
|
| 2025 |
ANXA7 acts as an adaptor protein facilitating retrograde transport of TIA1-containing ribonucleoprotein (RNP) granules by linking them to cytoplasmic dynein in axons; elevated axonal Ca2+ disrupts this linker role, causing detachment of TIA1 granules from dynein and pathological TIA1 aggregation; ANXA7 knockdown similarly impairs trafficking and causes axonopathy in vitro and in vivo. |
Live imaging of axonal RNP transport; ANXA7 knockdown and overexpression; Co-IP (ANXA7-TIA1-dynein); Ca2+ manipulation; in vitro and in vivo axonopathy models |
bioRxivpreprint |
Medium |
bio_10.1101_2025.01.16.633295
|
| 1999 |
ANX7/ANXA7 contains a PGQM motif in its regulatory domain; this motif is shared with HIV-1 Gag, and mutations in this motif in Gag disrupt viral replication, suggesting the motif mediates protein-protein interactions relevant to membrane fusion/secretory functions of ANXA7. |
Alanine scanning mutagenesis of PGQM motif in HIV-1 Gag; single- and multi-round viral replication assays; sequence homology with synexin/ANX7 |
Proceedings of the National Academy of Sciences of the United States of America |
Low |
10077575
|
| 2025 |
ANXA7 GTPase activation promotes lipid droplet formation and mitochondria-lipid droplet interaction by interacting with PPARγ to enhance its stability and promote its nuclear translocation; this leads to Perilipin 5 upregulation, NRF2 nuclear translocation, and GPX4 expression, thereby inhibiting oxidative stress and lipid peroxidation in spinal cord injury neurons. |
ANXA7 GTPase activation (small molecule); Co-immunoprecipitation (ANXA7-PPARγ); PPARγ stability assay; lipid droplet and mitochondria imaging; NRF2/GPX4 expression; SCI mouse model with CatWalk assay |
Advanced science |
Medium |
39996504
|