Disease relevance of CCL3L3

• Administration of the recombinant stem cell inhibitor molecule LD78 as an adjunct to chemotherapy has potential clinical benefit in reducing or preventing the neutropenia associated with this treatment [1].
• The response of normal and chronic myeloid leukemia (CML), CD34+ cells to human macrophage inflammatory protein-1 alpha (MIP-1 alpha or LD78) was assessed [2].
• LD78 gene transcripts were detected in eight of eight fresh samples of cells from patients with acute nonlymphocytic leukemia (ANLL) by Northern blot analysis [3].

High impact information on CCL3L3

• KG-1, HL-60, HUT 102, MT-2, and MJ cell lines expressed the LD78 gene constitutively [3].
• This protein was not found in culture supernatants or cell lysates of monocytic leukemia cells and HL-60 cells, although LD78 transcripts were found in those cells [3].
• The gene coding for the protein LD78 was isolated from stimulated human tonsillar lymphocytes by differential hybridization [3].
• Promoters of the LD78 alpha and LD78 beta genes showed similar inducible activities in two leukemic cell lines, K562 and Jurkat, but the induction mechanisms differed between the two cell lines [4].
• Cytokine LD78 is a human counterpart of the mouse macrophage inflammatory protein 1 alpha/hematopoietic stem cell inhibitor [4].

Biological context of CCL3L3

• In our analyses of cosmid clones, the LD78 beta gene and the second gene for AT744, which is also a member of the superfamily are closely linked in a head-to-head arrangement [5].
• Exons 2 and 3 and the intron between them are highly homologous to those of the LD78 beta gene, hence, the gamma gene was probably derived from the beta gene [5].
• Nucleotide sequence of the third cytokine LD78 gene and mapping of all three LD78 gene loci to human chromosome 17 [5].
• We cloned the third human gene for the LD78, termed LD78 gamma and the sequence analysis showed that it is a 5'-truncated pseudogene [5].
• The 4.2-kb fragment contained genomic DNA sequences corresponding to the LD78 cDNA and was named the LD78 alpha gene [6].

Anatomical context of CCL3L3

• Characterization of the quaternary structure and conformational properties of the human stem cell inhibitor protein LD78 in solution [1].
• Macrophage inflammatory protein (MIP)-1 alpha, also known as LD78, is a member of a family of chemokines which recruit leukocytes to sites of inflammation [7].
• 125I-labeled recombinant LD78 bound most efficiently to U937 cells [8].
• Treatment of human myeloid cell lines HL-60 and U937 with phorbol 12-myristate 13-acetate (PMA) increased within 2 h cellular levels of the RNA hybridizable to LD78 cDNA [6].
• Addition of cycloheximide had no apparent effect on this response in U937 cells and inhibited the response in fibroblasts, whereas it stimulated the response in HL-60 and U105MG cells. mRNA phenotyping experiments revealed that the LD78 alpha and LD78 beta genes were both transcribed in PMA-stimulated U937 cells [6].

Other interactions of CCL3L3

• These receptors for LD78 were distinct from the receptors for gamma-IFN and for IL-8 [8].

Analytical, diagnostic and therapeutic context of CCL3L3

• The hydrodynamic and structural properties of LD78 have been determined in various buffer solutions using analytical ultracentrifugation, circular dichroism, and fluorescence spectroscopy [1].
• Southern blot analysis of the EcoRI-digested human genomic DNAs, using previously isolated LD78 cDNA as a probe, showed that in each individual there are 4.2- and 4.8-kilobase-pair (kb) fragments and that some have an additional 6.5-kb fragment [6].
• The LD78 protein was detected in culture supernatants and cell lysates of HUT 102, MT-2, MJ, and fresh ATL cells by Western blot analysis [3].

References