Disease relevance of ITGB1

• The tumors showed immunoreactivity for CD18, CD29, and CD49d, but not for CD11a, mimicking the phenotype of human Epstein-Barr virus (EBV)-related lymphomas [1].
• METHODS: Flow-cytometric analyses for CD49d, CD29, and CD45RO were performed on T cell lines specific for timothy, tetanus, and Candida from atopic and nonatopic donors [2].
• Increased expression of adhesion molecules (CD54, CD29 and CD44) on fibroblasts infected with cytomegalovirus [3].
• Comparison between the different categories revealed that peripheral blood T cells from patients with multiple sclerosis expressed significantly lower amounts of the VLA integrins 4 and 5 as well as their common beta subunit CD29, compared with normal control subjects [4].
• We studied the changes in expression of CD9 and beta1-integrins (CD29, VLA) in human vascular smooth muscle cells (VSMCs) under in vitro culture conditions mimicking proliferative vascular diseases [5].

High impact information on ITGB1

• Fibulin, a novel protein that interacts with the fibronectin receptor beta subunit cytoplasmic domain [6].
• Immunofluorescent staining of cells cultured on fibronectin showed the 100 kd protein coinciding with the fibronectin receptor beta subunit in sites of substrate contact [6].
• We show here that an antibody which recognizes the beta-subunit of VLA-4 (CD29) on T cells can inhibit CD4+ cell proliferation triggered by CD2 or CD3, and that binding of this antibody to activated T cells leads to an increase in cyclic AMP levels which is comparable to that elicited by forskolin [7].
• These negative signalling effects are unique to this antibody: other CD29 antibodies do not affect the growth of activated CD4 cells but enhance the proliferation of whole T cell populations and abrogate the suppressive effects of mitomycin-treated CD8 cells on CD4-cell growth [7].
• Suppressor effects and cyclic AMP accumulation by the CD29 molecule of CD4+ lymphocytes [7].

Chemical compound and disease context of ITGB1

• In order to determine the cellular targets of AMI in human gastric cancer SC-M1 cells, we examined AMI-induced changes in the levels of adhesion molecules CD29 (beta 1 integrin) and CD54 (ICAM-1) and GSH [8].
• A family with MEN 2A, consisting of 88 members and their spouses, was studied to test the reliability of the provocation of plasma calcitonin with pentagastrin and the possibility of DNA diagnosis of mutated gene carriers with DNA probes closely linked to the MEN2A gene including RBP3 and FNRB genes [9].

Biological context of ITGB1

• CONCLUSION: PSMB6 and ITGB1 genes may be related to the differentiation and/or apoptosis of NB4 cells induced by As2O3 [10].
• In the present study we characterize the role of vascular endothelial growth factor (VEGF) and beta(1) integrin (CD29) in MM cell migration [11].
• Inclusion of an inhibitor of protein glycosylation and exocytosis (brefeldin A) at all stages of separation partially prevented an increase in the percentage of DCs bearing CD18, C29 and C54 whereas the inclusion of cycloheximide (an inhibitor of polypeptide synthesis) interfered with increases in the percentage of cells bearing CD29 and CD54 [12].
• CD44 (homing cell adhesion molecule) and very late activation antigen beta 1 (VLA beta 1; CD29) could be demonstrated on almost all fibroblasts without an alteration following cytokine stimulation [13].
• The crosslinking of VLA-beta 1 (CD29) with a specific monoclonal antibody (mAb) (anti-4B4) plus anti-mouse immunoglobulin resulted in the rapid tyrosine phosphorylation of a 105-kD protein (pp105) in the human T cell line H9, as well as in peripheral resting T cells [14].

Anatomical context of ITGB1

• These mast cells and the other cell types present also adhere spontaneously to fibronectin and to laminin, this adhesion being partially inhibited by antibodies against CD61 and CD29 integrins [15].
• CD29, CD18, and CD11a were also present on each of these cell lines [16].
• In the binding assays, the numbers of FDCs bound to fibronectin- and laminin-coated dishes and LFs of cryostat sections of human tonsils were reduced markedly by pretreatment with monoclonal antibodies against CD29, CD49e, and CD49f [17].
• Lymphocyte adhesion to the retinal vessels was more dependent on CD29 (the common chain of the beta 1 integrins) expression than either CD11a/CD18 or CD49d [18].
• Conversely, the integrity of the endothelial cells was underscored by their even reactivity for CD29, CD44, and CD54 [19].

Associations of ITGB1 with chemical compounds

• Both CD29 and CD49d clustering significantly inhibited anti-IgE-induced histamine release from the human basophil [20].
• Upregulated expression of VLA proteins and CD29 in peripheral blood lymphocytes of chronic alcoholics without ethanol-related diseases [21].
• The staining of CD 29 on keratinocytes of affected and unaffected psoriatic skin was not affected by cyclosporin [22].
• Aggregation induced by CD98 antibodies could be distinguished from that induced by beta1-integrin (CD29) ligation by lack of sensitivity to EDTA and by increased sensitivity to deoxyglucose [23].
• Characterization of the human platelet glycoprotein IIIa gene. Comparison with the fibronectin receptor beta-subunit gene [24].

Physical interactions of ITGB1

• Antibody to the integrin beta 1, chain (CD29) eliminated binding to collagen and laminin but not to fibronectin, fibroblasts, and HT-29 monolayers [25].

Regulatory relationships of ITGB1

• In contrast with the activating CD29 mAb 8A2, a combination of blocking CD49 mAbs or the nonactivating but blocking CD29 mAb AIIB2 failed to inhibit completely eosinophil migration over FN-preincubated or HUVEC-covered filters. mAb 8A2 stimulated binding to FN but not to HUVEC [26].
• The above results strongly suggest that the VLA/CD29 family of antigens may play an important role in regulating CD4 T cell activation via the CD3-T cell receptor pathway [27].
• However, a CD29 mAb which inhibits homotypic cell aggregation could not block this IL-8 production [28].
• Pretreatment of neutrophils with either a CD29-stimulating monoclonal antibody or the addition of TNF-alpha (0.1-10 U/ml) to the coculture failed to induce transendothelial migration [29].
• Monoclonal antibodies to beta1 integrins beta-subunit (CD29) also strongly induced tumor necrosis factor-alpha and interleukin-10 production, but not interleukin-12 [30].

Other interactions of ITGB1

• Immunoelectron microscopy revealed fibers surrounded by cytoplasmic FDC extensions that were CD29-, CD49e-, and CD49f-positive [17].
• Given that CD29 is currently regarded as critical for lymphocyte trafficking in general and for transvascular migration in particular, and CD54 is also involved in transvascular lymphocyte migration, we conclude that their consistent absence in IL may contribute to its intravascular and disseminated distribution pattern [19].
• In all cases, the surfaces of IL aggregates reacted for CD44 but were consistently negative for CD29; also absent was CD54 [19].
• No evidence for adhesion to vitronectin through CD29 and beta 5 integrins was obtained [15].
• Neutralizing antibodies reactive with either alpha 4, VCAM-1, or CD29 were all equally capable of inhibiting the binding of activated leukocytes to mesothelial cells (in the presence of anti-CD18 antibody) [31].

Analytical, diagnostic and therapeutic context of ITGB1

• Antibodies against VLA-4, CD29, and LFA-1 also inhibited the induced IL-6 secretion in plasma cell-LTBMC cocultures [32].
• MSCs of passage 3 were examined for the purify by positive rate of CD29 and CD44 through flow cytometry [33].
• Because VLA/CD29 is preferentially expressed on CD4 memory T cells, the above described system will be used to develop a novel drug design for providing selective immunosuppression useful for organ transplantation [34].
• A 100 kd protein was isolated from tissue and cell extracts by affinity chromatography on a synthetic peptide representing the cytoplasmic domain of the fibronectin receptor beta subunit [6].
• Dissection of the pGEM-32 clone demonstrated that the region revealing the non-chromosome-10 sequences is within a fragment about 1.7 kb in length extending from about 600 nucleotides preceding the stop codon down to the end of the cloned FNRB 3' untranslated region [35].

References