| 1990 |
CD53 is a 219-amino acid type III integral membrane protein with four transmembrane domains and N-glycosylation sites, constituting the structural basis of the tetraspanin family; it is the human homologue of rat OX-44. |
cDNA cloning, sequence analysis, immunoprecipitation of transfected cells |
Journal of immunology |
High |
1700763 2258620
|
| 1993 |
Cross-linking of CD53 on human B cells, monocytes, and granulocytes triggers cytoplasmic calcium fluxes and activates the monocyte oxidative burst; signaling is largely independent of protein kinase C but sensitive to high-dose staurosporine and dependent on tyrosine kinases rather than GTP-binding proteins. |
Cross-linking of cell-bound F(ab')2 anti-CD53 mAb; calcium flux assay; oxidative burst assay; pharmacological inhibitors (staurosporine, ADP-ribosylating toxins) |
Journal of immunology |
High |
8335905
|
| 1993 |
The major extracellular (hydrophilic) loop of CD53 contains epitopes recognized by anti-CD53 mAbs (OX-44, 2D1, 6E2, 7D2), and these epitopes are sensitive to reduction, demonstrating the importance of disulfide bonding in the correct folding of the CD53 extracellular domain and directly confirming the four-transmembrane topology. |
Epitope mapping using GST-fusion chimeric proteins and anti-rat CD53 mAbs; reduction sensitivity assays |
European journal of immunology |
High |
7678222
|
| 1994 |
CD53 (together with CD37, TAPA-1/CD81, and R2/C33) co-precipitates with MHC class II (DR) glycoproteins from B cell lysates in mild detergent, forming large multicomponent complexes on the B cell surface. |
Co-immunoprecipitation and preclearing experiments from human B-cell line and tonsillar B cell lysates |
Immunogenetics |
High |
8119731
|
| 1994 |
Activation of CD53 in rat macrophages by antibody cross-linking increases inositol phosphates, diacylglycerol, and intracellular Ca2+ (insensitive to pertussis/cholera toxins), leads to protein kinase C translocation to the membrane, and induces expression of inducible nitric oxide synthase (iNOS) resulting in nitric oxide release in a PKC- and protein synthesis-dependent manner. |
Antibody cross-linking; inositol phosphate and diacylglycerol measurement; Ca2+ mobilization; PKC translocation assay; NO measurement; iNOS expression analysis; pharmacological inhibitors |
The Journal of experimental medicine |
High |
7511680
|
| 1994 |
Cross-linking of CD53 on resting human B lymphocytes promotes their entry into G1 phase (increased CD69, cell volume, RNA synthesis, c-myc levels), and in combination with cytokines (IL-2, IL-4) induces DNA synthesis and immunoglobulin production. |
Anti-CD53 mAb cross-linking; flow cytometry; RNA synthesis measurement; c-myc immunoblot; [3H]thymidine incorporation; Ig ELISA |
Journal of immunology |
High |
7963560
|
| 1995 |
Immune complexes of rat CD53 contain tyrosine phosphatase activity capable of dephosphorylating Lck in vitro; the phosphatase is distinct from CD45 and is inhibited by tyrosine phosphatase inhibitors. CD63 similarly co-precipitates a phosphatase. |
Immunoprecipitation from lymph node and thymoma lysates; in vitro phosphatase activity assay on phospho-Lck and synthetic substrate; depletion experiments; phosphatase inhibitor treatment |
European journal of immunology |
Medium |
7621882
|
| 1996 |
CD53, CD82, CD63, and CD81 specifically associate with integrin α4β1 (VLA-4/CD49d/CD29) on hematopoietic cell lines, as shown by reciprocal co-immunoprecipitation; the association is independent of the α4 cytoplasmic domain and divalent cations but is lost in two α4 adhesion-deficient mutants (D346E and D408E). |
Reciprocal co-immunoprecipitation; confocal microscopy; mutant integrin transfectants; divalent cation chelation |
Journal of immunology |
High |
8757325
|
| 1996 |
CD53, CD81, and CD82 are in close proximity (2–10 nm) to MHC class II (DR, DQ), MHC class I, and CD20 on B cell surfaces, forming supramolecular complexes; FRET analysis suggests all these molecules participate in a single multi-component assembly. |
Flow cytometric FRET (fluorescence energy transfer) with fluorescently labeled mAbs |
Journal of immunology |
High |
8816400
|
| 1997 |
CD53 ligation on lymphoma B cells (rat IR938F) induces homotypic adhesion that requires divalent cations (Ca2+, Mg2+), de novo protein synthesis, and is mediated by tyrosine kinase (genistein/piceatannol-sensitive), PI3K (wortmannin-sensitive), and PKC (H7/bisindolylmaleimide-sensitive) signaling pathways, but is LFA-1-independent; electron microscopy reveals localized membrane contact zones. |
Anti-CD53 mAb cross-linking; cell aggregation assay; pharmacological inhibitors (genistein, piceatannol, wortmannin, H7, bisindolylmaleimide, cycloheximide, actinomycin D, EGTA/EDTA); immunoelectron microscopy |
Cellular immunology |
High |
9225004
|
| 1997 |
Anti-CD53 mAb induces homotypic aggregation of lymphoid cell lines via both LFA-1/ICAM-1-dependent and -independent pathways; aggregation is energy-dependent and partially blocked by anti-LFA-1 or anti-ICAM-1, but not by anti-CD44 or anti-CD49d mAbs. |
Anti-CD53 mAb cross-linking; blocking mAb experiments; cell aggregation assay including a LAD patient B cell line lacking LFA-1 |
Immunobiology |
Medium |
9241532
|
| 1997 |
Anti-CD53 mAb (like anti-CD9, anti-CD81, anti-CD82 mAbs) delivers a costimulatory signal for CD3-mediated T cell activation and inhibits migration of megakaryocytic and pre-B cell lines, consistent with CD53 participation in a tetraspan network. |
mAb cross-linking; T cell costimulation assay; homotypic aggregation and migration inhibition assays in HEL and NALM-6 cell lines |
Cellular immunology |
Medium |
9514697
|
| 1998 |
Physiological neutrophil activators (TNFα, PAF, fMLP, PMA, ionomycin) cause down-regulation of CD53 from the neutrophil cell surface via a proteolytic mechanism (inhibited by PMSFP), without changes in CD53 transcript levels. |
Flow cytometry; immunoblotting; pharmacological inhibition (PMSF); Northern/RT analysis |
Journal of leukocyte biology |
Medium |
9620662
|
| 2002 |
Ligation of CD53 (rat or human) induces a transient 3–4-fold activation of JNK that peaks at 3–5 min in B-cell lymphoma and T-cell lymphoma lines, and in a renal carcinoma line transiently transfected with human CD53; this JNK activation is independent of Vav and sufficient to stimulate Jun-dependent transcription. |
Anti-CD53 mAb cross-linking; in vitro JNK kinase assay (endogenous and exogenous); Jun-dependent transcriptional reporter; Vav co-stimulation assay |
European journal of biochemistry |
Medium |
11846804
|
| 2003 |
CD53 ligation on tumor B and T cells (IR938F, Jurkat) reduces apoptosis induced by serum deprivation, decreases caspase activation and DNA fragmentation, increases Bcl-xL and decreases Bax, and activates AKT (phosphorylation at Ser473). |
Anti-CD53 mAb cross-linking; PARP cleavage assay; DNA fragmentation assay; Bcl-xL/Bax immunoblot; AKT phosphorylation immunoblot |
Oncogene |
High |
12606948
|
| 2003 |
CD53 ligation in rat mesangial cells triggers DNA synthesis via ERK1/ERK2 activation (blocked by PD98059/MEK inhibitor), but not through PI3K, PKC, or calcium channel pathways; CD53 is expressed in mesangial cells in vivo. |
Anti-CD53 mAb cross-linking; [3H]thymidine incorporation; ERK phosphorylation by immunoblot; pharmacological inhibitors (PD98059, wortmannin, PKC inhibitors, thapsigargin, verapamil); flow cytometry for apoptosis |
Kidney international |
Medium |
12631118
|
| 2004 |
CD53 overexpression in macrophages increases intracellular GSH, lowers peroxide levels, and confers resistance to H2O2 and UVB irradiation; antisense CD53 has the opposite effects; CD53 is induced by LPS and nitric oxide (SNAP) in macrophages. |
Stable sense and antisense CD53 transfection; GSH measurement; peroxide assay; H2O2 and UVB cell viability assays; Northern blot; microarray |
Molecules and cells |
Medium |
15055538
|
| 2007 |
In macrophages, HIV-1 buds into an intracellular plasma membrane domain containing tetraspanins CD81, CD9, and CD53 (not classic endosomes); this compartment is connected to the cell surface (accessible to extracellular tracers at 4°C) and lacks endosome markers including CD63. |
Immunofluorescence microscopy; immunoelectron microscopy; horseradish peroxidase and ruthenium red tracer accessibility assays; marker co-localization |
The Journal of cell biology |
High |
17438075
|
| 2007 |
CD53 gene expression is directly regulated by the transcription factor EBF1; functional EBF1 binding sites are present in the CD53 promoter and EBF1 expression drives CD53 transcription in transient transfection assays. |
Retroviral EBF1 transduction of BaF/3 cells; microarray; promoter 5' end mapping; transient transfection transcriptional assays |
European journal of immunology |
Medium |
17429843
|
| 2013 |
CD53 knockdown by siRNA in THP-1 monocytic cells stimulated with house dust mite significantly increases production of inflammatory cytokines and NFκB activity, demonstrating that CD53 suppresses over-activation of inflammatory cytokine responses. |
siRNA knockdown; cytokine ELISA; NFκB activity assay |
Biochimica et biophysica acta |
Medium |
23313165
|
| 2014 |
CD53 ligation on rat NK cells reduces degranulation and IFNγ responses to activating NK receptors (Ly49s3, NKR-P1A, NKp46), induces activation of the β2 integrin LFA-1, promotes homotypic NK cell adhesion, and enhances NK cell proliferation in response to IL-2. |
Anti-CD53 mAb cross-linking; degranulation assay; redirected killing assay; IFNγ ELISA; LFA-1 activation flow cytometry; proliferation assay |
PloS one |
Medium |
24832104
|
| 2019 |
CD53 physically interacts with IL-7Rα and promotes IL-7 signaling (PI3K and JAK/STAT pathways) in developing B cells; loss of CD53 reduces IL-7Rα surface expression, increases apoptosis in pro-B cells, and blocks the pro-B to pre-B transition. |
Co-immunoprecipitation; proximity ligation assay; flow cytometry for IL-7Rα; phospho-flow for PI3K and JAK/STAT; apoptosis assays; mixed bone marrow chimeras |
Journal of immunology |
High |
31748347
|
| 2020 |
CD53 stabilizes L-selectin surface expression on B and T cells, restrains L-selectin shedding via both ADAM17-dependent and ADAM17-independent mechanisms, and is required for efficient lymphocyte homing to lymph nodes; Cd53−/− mice have markedly smaller lymph nodes due to reduced B and T cell homing. |
Cd53−/− mouse analysis; flow cytometry for L-selectin; adoptive transfer homing assays; ADAM17 inhibitor experiments; in vivo lymph node cellularity |
iScience |
High |
32428859
|
| 2020 |
CD53 restrains α3 integrin mobilization in neutrophils, promotes cytoskeletal remodeling and transendothelial migration; Cd53−/− neutrophils show defective transmigration across endothelium in response to TNF, CXCL1, and CCL2, and near-complete absence of L-selectin. |
Cd53−/− mouse; intravital microscopy; peritoneal inflammation model; flow cytometry for adhesion molecules and integrins; cytoskeletal remodeling assays; serum-induced arthritis model |
Journal of immunology |
High |
32532837
|
| 2022 |
CD53 interacts with CD45 (identified by unbiased mass spectrometry) and is required for CD45RO isoform expression, CD45 membrane stability and mobility, and optimal CD45 phosphatase activity, leading to Lck activation; Cd53−/− T cells show proliferation defects and impaired tumor rejection. |
Unbiased mass spectrometry; proximity ligation assay; FRAP (fluorescence recovery after photobleaching); phosphatase activity assay; Lck activation immunoblot; in vivo tumor rejection model; IFNγ ELISPOT |
Cell reports |
High |
35767951
|
| 2022 |
CD53 integrates inflammatory and metabolic signals in hepatocytes; CD53 deletion blocks Western diet-induced dyslipidemia, hepatic inflammatory gene expression, and triglyceride accumulation; CD53 deletion attenuates TNFα- and fatty acid+LPS-induced cytokine expression in isolated hepatocytes. |
Germline CD53 KO mice; Western diet feeding; NASH diet model; primary hepatocyte isolation; cytokine gene expression; triglyceride assay; glucose transporter 8 deletion and trehalose treatment as comparators |
The Journal of biological chemistry |
Medium |
36581203
|
| 2023 |
CD53 interacts with DREAM complex-associated proteins, specifically promoting the interaction between Rbl2/p130 and its phosphatase PP2A, stabilizing p130 for DREAM complex assembly; this promotes HSC quiescence following inflammatory stress, and loss of CD53 leads to prolonged cycling and reduced HSC function. |
Proximity labeling proteomics; confocal fluorescence microscopy; DREAM complex co-immunoprecipitation; PP2A-p130 interaction assay; Cd53−/− HSC cell cycle analysis; 5-FU stress model |
Blood |
High |
36542833
|
| 2023 |
Glycosylation of CD53 inhibits its interaction with partner proteins CD45, CD20, and CD37; abrogation of CD53 glycosylation does not affect surface expression but increases interaction with partners. CD37 glycosylation is required for its surface expression, while CD53 glycosylation controls partner protein interaction capacity. |
Glycosylation mutant generation; surface expression flow cytometry; single-molecule dSTORM super-resolution microscopy; co-immunoprecipitation |
Biophysical journal |
Medium |
38031400
|
| 2024 |
CD53 physically interacts with CXCR4 (confirmed by proximity ligation assay) and promotes CXCL12-induced CXCR4 signaling and receptor internalization; Cd53−/− B cells show reduced CXCL12 migration in vitro and impaired bone marrow homing in vivo. |
Proximity ligation assay; in vitro migration assay; CXCR4 signaling (phospho-flow); CXCR4 internalization assay; in vivo homing assay in Cd53−/− mice |
Journal of immunology |
High |
38363205
|
| 2024 |
The 'closed' conformational mutant of CD53 (F44E) shows increased clustering in nanodomains and greater interaction with its partner CD45 compared to wild-type CD53; absence of CD53 increases CD45 clustering tendency, indicating CD53 conformation regulates its nanoscale membrane organization and partner interactions. |
Conformational mutant generation (F44E); super-resolution dSTORM microscopy; co-immunoprecipitation; CD53 KO B cells |
The Journal of biological chemistry |
Medium |
39159818
|
| 2025 |
CD53 promotes ROS-induced neutrophil extracellular trap (NET) formation via modulation of the PI3K/AKT pathway; anti-CD53 neutralizing antibody inhibits NET formation in vitro and reduces inflammatory injury in a caerulein-induced acute pancreatitis mouse model. |
PMA-induced in vitro NET model; anti-CD53 neutralizing antibody; PI3K/AKT pathway analysis; caerulein AP mouse model; NET quantification in tissues |
Journal of inflammation research |
Medium |
40098997
|