Key Spec Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|Description||Anti-MIP-1 β/CCL4 (CT) Antibody, rabbit monoclonal|
|Presentation||In 60% storage buffer (50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 0.01% sodium azide and 0.05% BSA) and 40% glycerol.|
|Application||This Anti-MIP-1 β/CCL4 (C-term) Antibody is validated for use in WB for the detection of MIP-1 β/CCL4 (C-term).|
|Safety Information according to GHS|
|Material Size||100 µL|
|Anti-MIP-1 beta/CCL4 (C-term), Rabbit monoclonal - 0611046355||0611046355|
|Reference overview||Pub Med ID|
|Transcription-dependence of histone H3 lysine 27 trimethylation at the Arabidopsis polycomb target gene FLC.|
Diana Mihaela Buzas,Masumi Robertson,E Jean Finnegan,Chris A Helliwell
The Plant journal : for cell and molecular biology 65 2011
The FLC gene encodes a MADS box repressor of flowering that is the main cause of the late-flowering phenotype of many Arabidopsis ecotypes. Expression of FLC is repressed by vernalization; maintenance of this repression is associated with the deposition of histone 3?K27 trimethylation (H3K27me3) at the FLC locus. However, whether this increased H3K27me3 is a consequence of reduced FLC transcription or the cause of transcriptional repression is not well defined. In this study we investigate the effect of changes in transcription rate on the abundance of H3K27me3 in the FLC gene body, a chromatin region that includes sequences required to maintain FLC repression following vernalization. We show that H3K27me3 is inversely correlated with transcription across the FLC gene body in a range of ecotypes and mutants with different flowering times. We demonstrate that the FLC gene body becomes marked with H3K27me3 in the absence of transcription. When transcription of the gene body is directed by an inducible promoter, H3K27me3 is removed following activation of transcription and H3K27me3 is added after transcription is decreased. The rate of addition of H3K27me3 to the FLC transgene following inactivation of transcription is similar to that observed in the FLC gene body following vernalization. Our data suggest that reduction of FLC transcription during vernalization leads to an increase of H3K27me3 levels in the FLC gene body that in turn maintains FLC repression.
|Natural truncation of the chemokine MIP-1 beta /CCL4 affects receptor specificity but not anti-HIV-1 activity.|
Guan, Ennan, et al.
J. Biol. Chem., 277: 32348-52 (2002) 2002
Activated lymphocytes synthesize and secrete substantial amounts of the beta-chemokines macrophage inflammatory protein (MIP)-1 alpha/CCL3 and MIP-1 beta/CCL4, both of which inhibit infection of cells with human immunodeficiency virus type 1 (HIV-1). The native form of MIP-1 beta secreted by activated human peripheral blood lymphocytes (MIP-1 beta(3-69)) lacks the two NH(2)-terminal amino acids of the full-length protein. This truncated form of MIP-1 beta has now been affinity-purified from the culture supernatant of such cells, and its structure has been confirmed by mass spectrometry. Functional studies of the purified protein revealed that MIP-1 beta(3-69) retains the abilities to induce down-modulation of surface expression of the chemokine receptor CCR5 and to inhibit the CCR5-mediated entry of HIV-1 in T cells. Characterization of the chemokine receptor specificity of MIP-1 beta(3-69) showed that the truncated protein not only shares the ability of intact MIP-1 beta to induce Ca(2+) signaling through CCR5, but unlike the full-length protein, it also triggers a Ca(2+) response via CCR1 and CCR2b. These results demonstrate that NH(2)-terminally truncated MIP-1 beta functions as a chemokine agonist with expanded receptor reactivity, which may represent an important mechanism for regulation of immune cell recruitment during inflammatory and antiviral responses.
|Molecular cloning of S-protein, a link between complement, coagulation and cell-substrate adhesion|
Jenne, D and Stanley, K K
EMBO J, 4:3153-7 (1985) 1985