| 1990 |
CD53 is a 219-amino acid integral membrane protein with four putative transmembrane domains and three N-glycosylation sites, structurally related to CD9, CD37, CD63, and TAPA-1 (tetraspan family). Protein sequence was deduced from cDNA cloning and confirmed by immunostaining/immunoprecipitation of transfected cells. |
cDNA cloning, sequence analysis, immunostaining and immunoprecipitation of transfected NIH3T3/COS cells |
Journal of immunology / Immunogenetics |
High |
1700763 2258620
|
| 1993 |
Cross-linking of CD53 on human B cells, monocytes, and granulocytes induces cytoplasmic calcium fluxes; in monocytes it also activates the oxidative burst. The signaling is largely protein kinase C-independent (not blocked by low staurosporine) but sensitive to high staurosporine and not blocked by ADP-ribosylating toxins, suggesting dependence on tyrosine kinases rather than GTP-binding proteins. |
Cross-linking with F(ab')2 anti-CD53 mAb + secondary antibody; calcium flux measurement; oxidative burst assay; pharmacological inhibitors (staurosporine, pertussis/cholera toxins) |
Journal of immunology |
Medium |
8335905
|
| 1994 |
CD53 activation by cross-linking in rat macrophages increases inositol phosphates, diacylglycerol, and Ca2+ mobilization (insensitive to pertussis/cholera toxins), causes PKC translocation to the membrane, and induces nitric oxide release via expression of inducible nitric oxide synthase (iNOS) in a PKC- and protein synthesis-dependent manner. |
Cross-linking of CD53 with mAb; measurement of inositol phosphates, DAG, Ca2+; PKC translocation assay; NO production assay; iNOS protein synthesis inhibition |
The Journal of experimental medicine |
Medium |
7511680
|
| 1994 |
CD53, CD37, TAPA-1, and R2/C33 tetraspanins co-precipitate with MHC class II DR antigens from B-cell lysates, forming large multicomponent complexes also containing CD19 and CD21. Shown by coprecipitation and preclearing experiments. |
Co-immunoprecipitation from mild detergent lysates of human B-cell lines and tonsillar B cells |
Immunogenetics |
Medium |
8119731
|
| 1994 |
Cross-linking of CD53 on resting human B cells promotes G1 cell cycle entry (increased CD69, RNA synthesis, c-myc, cell volume) and, in cooperation with IL-2 or IL-4, induces DNA synthesis and Ig production, demonstrating a functional role in B cell activation. |
Anti-CD53 mAb cross-linking; flow cytometry for CD69; RNA synthesis measurement; c-myc Western blot; DNA synthesis (7-AAD binding); Ig ELISA |
Journal of immunology |
Medium |
7963560
|
| 1995 |
Immunoprecipitates of rat CD53 from lymph node and thymoma cell lysates contain tyrosine phosphatase activity capable of dephosphorylating the tyrosine kinase Lck and a synthetic phosphotyrosine substrate in vitro; activity is abrogated by a tyrosine phosphatase inhibitor. The associated phosphatase is not CD45 (shown by depletion experiments). |
Co-immunoprecipitation; in vitro phosphatase activity assay on Lck and synthetic substrate; depletion experiments; phosphatase inhibitor treatment |
European journal of immunology |
Medium |
7621882
|
| 1996 |
CD53, CD63, and CD82 (like CD81/TAPA-1) specifically co-precipitate with integrin α4β1 (CD49d/CD29) from hemopoietic cell lines; the association does not require the α4 cytoplasmic domain or divalent cations, but two α4 adhesion-deficient mutants (D346E, D408E) lack this association. |
Reciprocal co-immunoprecipitation from multiple α4β1-positive cell lines; confocal microscopy for colocalization; mutant integrin analysis |
Journal of immunology |
High |
8757325
|
| 1996 |
CD53, CD81, and CD82 are in close proximity (within 2–10 nm) with MHC class II (DR, DQ), MHC class I, and CD20 at the B cell surface, forming a single large supramolecular complex as determined by FRET analysis. |
Flow cytometric FRET (fluorescence resonance energy transfer) with labeled mAbs on JY B cells |
Journal of immunology |
Medium |
8816400
|
| 1997 |
CD53 ligation induces homotypic adhesion in rat B-cell lymphoma that requires de novo protein synthesis (blocked by cycloheximide/actinomycin D), divalent cations (Ca2+/Mg2+), and is dependent on tyrosine kinases (genistein/piceatannol-sensitive), PI3K (wortmannin-sensitive), and PKC (H7/bisindolylmaleimide-sensitive), but not LFA-1. |
Anti-CD53 mAb (MRC OX-44) stimulation; pharmacological inhibitors; electron microscopy of cell contact zones |
Cellular immunology |
Medium |
9225004
|
| 1998 |
Physiological activators of neutrophils (TNFα, PAF, fMLP, PMA, ionomycin) cause down-regulation of CD53 from the neutrophil surface without changing CD53 mRNA levels; this down-regulation is blocked by the serine protease inhibitor PMSF, indicating proteolytic shedding. |
Flow cytometry; immunoblotting; Northern blot; PMSF protease inhibitor treatment of human neutrophils |
Journal of leukocyte biology |
Medium |
9620662
|
| 2002 |
CD53 ligation (rat or human) induces a 3–4-fold transient activation of JNK kinase activity (peak 3–5 min) in B-cell and T-cell lymphoma lines, and in renal carcinoma cells transiently transfected with human CD53 cDNA. JNK activation is not mediated by Vav, and CD53 does not cooperate with CD3 for Vav activation. In stable CD53-transfected cells, JNK activation stimulates Jun-dependent transcriptional activity. |
JNK kinase activity assay on endogenous and transfected cells; transcriptional reporter assay; pharmacological and genetic controls |
European journal of biochemistry |
Medium |
11846804
|
| 2003 |
CD53 ligation on tumor lymphoma cells triggers a survival signal reducing apoptosis by activating AKT (phospho-Ser473), increasing Bcl-xL levels, decreasing Bax levels (changing Bcl-xL/Bax ratio ~24-fold toward survival), and reducing caspase activation and DNA fragmentation. |
Anti-CD53 mAb ligation; Western blot for phospho-AKT, Bcl-xL, Bax; PARP cleavage assay; DNA fragmentation assay; serum deprivation model |
Oncogene |
Medium |
12606948
|
| 2003 |
CD53 ligation on primary rat mesangial cells induces DNA synthesis via ERK1/ERK2 activation; this effect is blocked by the MEK inhibitor PD98059 but not by PI3K, PKC inhibitors, or calcium channel blockers, defining a specific ERK-dependent mitogenic pathway. |
Thymidine incorporation; ERK phosphorylation by Western blot; pharmacological inhibitors (PD98059, wortmannin, H7, thapsigargin, verapamil); flow cytometry |
Kidney international |
Medium |
12631118
|
| 2004 |
Stable overexpression of CD53 in macrophages increases intracellular glutathione (GSH) and decreases peroxide levels, conferring resistance to H2O2 and UVB irradiation; antisense CD53 has the opposite effect. CD53 is also induced by LPS and nitric oxide (SNAP) in RAW264.7 macrophages. |
Stable transfection (sense and antisense CD53); GSH measurement; peroxide assay; H2O2 and UVB survival assays; microarray + Northern blot for induction |
Molecules and cells |
Medium |
15055538
|
| 2007 |
In macrophages, HIV-1 assembles into an intracellular plasma membrane domain that contains tetraspanins CD81, CD9, and CD53 (but not endosome marker CD63). These CD53/CD81/CD9-positive compartments are connected to the cell surface (accessible to HRP/ruthenium red at 4°C), indicating they are an internalized plasma membrane domain, not endosomes. CD63 is secondarily recruited to the virus-containing compartment. |
Immunofluorescence microscopy; immunoelectron microscopy; horseradish peroxidase/ruthenium red tracer accessibility assays; tetraspanin co-localization in HIV-infected macrophages |
The Journal of cell biology |
High |
17438075
|
| 2007 |
CD53 is a direct transcriptional target of the early B cell factor EBF1; functional EBF1 binding sites were identified in the CD53 promoter and confirmed to respond to EBF1 expression in transient transfection assays. |
Retroviral EBF1 overexpression in BaF/3 cells + microarray; promoter mapping; transient transfection reporter assay |
European journal of immunology |
Medium |
17429843
|
| 2013 |
siRNA knockdown of CD53 in THP-1 monocytic cells stimulated with house dust mite antigen leads to over-activation of inflammatory cytokine production and increased NF-κB activity, demonstrating that CD53 acts as a suppressor of inflammatory cytokine signaling. |
siRNA knockdown; cytokine ELISA; NF-κB activity assay; promoter polymorphism functional analysis (EMSA) |
Biochimica et biophysica acta |
Medium |
23313165
|
| 2014 |
CD53 ligation on rat NK cells reduces degranulation and IFN-γ response to activating receptors (Ly49s3, NKR-P1A, NKp46), induces LFA-1 activation and homotypic NK cell adhesion, and enhances NK cell proliferation in response to IL-2, indicating CD53 modulates NK cell effector functions by promoting adhesion over cytotoxicity. |
Anti-CD53 mAb ligation; degranulation assay (CD107a); redirected killing assay; IFN-γ ELISA; LFA-1 activation assay (conformational mAb); proliferation assay |
PloS one |
Medium |
24832104
|
| 2019 |
CD53 promotes IL-7 receptor (IL-7Rα) surface expression and downstream PI3K and JAK/STAT signaling in prepro- and pro-B cells; CD53-deficient mice have reduced IL-7Rα surface expression, impaired IL-7 signaling, increased apoptosis in developing B cells, and a block at the pro-B to pre-B cell transition. CD53 physically interacts with IL-7R as shown by co-immunoprecipitation and proximity ligation assay. |
Cd53-/- mouse model; mixed bone marrow chimeras; flow cytometry; phospho-signaling (PI3K, JAK/STAT) assays; co-immunoprecipitation; proximity ligation assay (PLA) |
Journal of immunology |
High |
31748347
|
| 2020 |
CD53 stabilizes L-selectin surface expression on lymphocytes and restrains its shedding via ADAM17-dependent and ADAM17-independent mechanisms. Loss of CD53 in mice results in near absence of L-selectin from B cells and reduced L-selectin stability on T cells, causing impaired lymphocyte homing to lymph nodes and defective antigen-dependent immune responses. |
Cd53-/- mouse model; flow cytometry for L-selectin; ADAM17 inhibitor experiments; adoptive transfer homing assays; intravital microscopy; human lymphocyte analysis |
iScience |
High |
32428859
|
| 2020 |
CD53 deficiency in mice impairs neutrophil transendothelial migration induced by TNF, CXCL1, and CCL2, reduces leukocyte retention under shear flow, and causes defects in activation-induced cytoskeletal remodeling. CD53-deficient neutrophils show increased α3 integrin expression and near-complete loss of L-selectin, and demonstrate delayed onset of serum-induced arthritis. |
Cd53-/- mouse model; intravital microscopy; peritoneal recruitment assays; adhesion molecule flow cytometry; cytoskeletal remodeling imaging; serum-induced arthritis model |
Journal of immunology |
High |
32532837
|
| 2022 |
CD53 is identified by unbiased mass spectrometry as a partner of CD45. CD53 controls CD45RO isoform expression and membrane mobility, stabilizes total CD45 on the membrane, and is required for optimal CD45 phosphatase activity and subsequent Lck activation. CD53-deficient T cells show substantial proliferation defects and impaired tumor rejection. |
Cd53-/- mouse model; unbiased mass spectrometry interactome; super-resolution microscopy (membrane mobility); phosphatase activity assay; Lck phosphorylation (Western blot); tumor rejection assay; IFN-γ intracellular staining |
Cell reports |
High |
35767951
|
| 2022 |
CD53 in hepatocytes integrates inflammatory and nutritional signals: high-fat/fructose exposure and inflammatory stimuli induce CD53 expression in liver; CD53 deletion in mice blocks Western diet-induced dyslipidemia, hepatic inflammatory transcriptome activation, adipose inflammation, and liver lipid accumulation. In isolated hepatocytes, CD53 deletion attenuates TNFα- and fatty acid+LPS-induced cytokine expression and triglyceride accumulation. |
Cd53-/- mouse model on Western/NASH diet; primary hepatocyte cultures with siRNA/KO; triglyceride assays; cytokine gene expression; transcriptomic analysis; glucose transporter 8 KO epistasis |
The Journal of biological chemistry |
Medium |
36581203
|
| 2023 |
CD53 promotes DREAM transcriptional repressor complex activity in hematopoietic stem cells (HSCs) by facilitating the interaction between Rbl2/p130 and its phosphatase PP2A, stabilizing p130 for DREAM binding and thereby promoting quiescence. Loss of CD53 causes prolonged cycling and reduced HSC function under inflammatory stress. |
Cd53-/- mouse model; proximity labeling (BioID); confocal fluorescence microscopy; DREAM complex co-immunoprecipitation; cell cycle analysis; HSC functional assays under inflammatory stress |
Blood |
High |
36542833
|
| 2023 |
Glycosylation of CD53 inhibits its interaction with partner proteins CD45, CD20, and CD37 (but not vice versa for CD37-CD53); surface expression of CD53 is unaffected by glycosylation. Conformational mutations show that the nanoscale clustering of CD53 depends on its conformation (closed mutant F44E shows higher clustering fraction). |
N-glycosylation mutants; surface expression flow cytometry; co-immunoprecipitation; dSTORM super-resolution microscopy |
Biophysical journal |
Medium |
38031400
|
| 2024 |
CD53 physically interacts with CXCR4 (the CXCL12 receptor) on B cells as shown by proximity ligation assay. CD53-deficient B cells show reduced CXCL12-induced CXCR4 signaling and receptor internalization, and impaired bone marrow homing in vivo. |
Proximity ligation assay; in vitro migration assay toward CXCL12; CXCR4 internalization assay; in vivo bone marrow homing assay in Cd53-/- mice |
Journal of immunology |
High |
38363205
|
| 2025 |
CD53 promotes neutrophil extracellular trap (NET) formation through the PI3K/AKT pathway; CD53 neutralizing antibody inhibits PMA-induced NETs in vitro and reduces inflammatory injury and NET formation in an acute pancreatitis mouse model. |
Anti-CD53 neutralizing antibody; in vitro NET model (PMA stimulation); PI3K/AKT pathway inhibitors; caerulein-induced AP mouse model; neutrophil isolation from AP patients |
Journal of inflammation research |
Medium |
40098997
|