Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0393754 (
HSA
)
2,996
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In a previous study, we raised a mAb (
MTS
35) reacting with a plasma membrane Ag expressed on both cortical thymocytes and a subset of thymic medullary epithelial cells. In view of the shared expression of this molecule, we have defined it as thymic shared Ag-1 (TSA-1). Considering its selective reactivity with cortical, but not medullary thymocytes, the relevance of TSA-1 as a marker of immature T cells was investigated in detail in this study, using multicolor flow cytometric analysis. TSA-1 was found on all immature thymocyte subsets (CD3-4-8-, CD3-4+8-, CD3-4-8+, CD3-4+8+, CD3low4+8+). Conversely, CD3high4+8- and CD3high4-8+ thymocytes, early thymic migrants and peripheral T cells were TSA-1-. More refined gating and analysis of the transitional CD3intermediate/high4+8+ thymocytes, proposed candidates for negative selection, demonstrated that approximately one half were TSA-1-. In fact, there was a directly inverse relationship between TSA-1 and CD3 expression on thymocytes. In the periphery, TSA-1 was detected on B lymphocytes. TSA-1 is PI-linked and has a molecular mass of 17 kDa nonreduced, or 12 to 13 kDa reduced. Through cross-correlation analysis, this molecule was distinct from H-2K, PNA-R, CD5, CD11a/18, Thy-1,
HSA
, Ly6A/E, Ly6C, ThB, CD25, CD44. Hence TSA-1 appears to be a unique marker which exquisitely separates mature from immature thymocytes.
...
PMID:Thymic shared antigen-1. A novel thymocyte marker discriminating immature from mature thymocyte subsets. 153 95
Using a modular library format in conjunction with cell viability (
MTS
) and flow cytometry assays, 90 cationic complexes [Au
PL
]
n
+
(
P
= phosphine ligand;
L
= thiourea derivative or chloride) were studied for their antiproliferative activity in CD8
+
T lymphocyte cells. The activity of the compounds correlates with the steric bulk of the phosphine ligands. Thiourea serves as a leaving group that is readily replaced by cysteine thiol (NMR, ESI-MS). Taking advantage of selective thiourea ligand exchange, the fragments [Au(PEt
3
)]
+
and [Au(JohnPhos)]
+
(JohnPhos = 1,1'-biphenyl-2-yl)di-
tert
-butylphosphine) in compounds
1
and
2
were transferred to recombinant human serum albumin (rHSA). PEt
3
promoted efficient modification of Cys34 in
HSA
(
HSA
-1
), whereas use of bulky JohnPhos as a carrier ligand led to serum protein nonspecifically modified with multiple gold adducts (
HSA
-2
) (Ellman's test, ESI-TOF MS).
HSA-1
, but not
HSA-2
, strongly inhibits T cell proliferation at nanomolar doses. The potential role of
HSA
as a delivery vehicle in gold-based autoimmune disease treatment is discussed.
...
PMID:Human Serum Albumin-Delivered [Au(PEt
3
)]
+
Is a Potent Inhibitor of T Cell Proliferation. 2852 13
