PMID- 10564822
OWN - NLM
STAT- MEDLINE
DCOM- 20000111
LR  - 20200213
IS  - 0378-1119 (Print)
IS  - 0378-1119 (Linking)
VI  - 240
IP  - 1
DP  - 1999 Nov 15
TI  - Cloning of DLM-1, a novel gene that is up-regulated in activated macrophages,
      using RNA differential display.
PG  - 157-63
AB  - Tumors interact with their environment, reprogramming host cells to induce
      responses such as angiogenesis, inflammation, immunity and immune suppression. To
      understand these processes, it is important to identify and isolate new genes
      whose expression is induced in host tissues in response to tumors. Ascites tumors
      offer an attractive model for isolating such genes, because responding host
      peritoneal lining tissues can be cleanly separated from tumor cells growing in
      suspension within the peritoneal cavity. We here report the cloning by
      differential display of a novel gene, DLM-1, that is highly up-regulated in the
      peritoneal lining tissue of mice bearing MOT ascites tumors. Mouse peritoneal
      macrophages, stimulated by IFN-gamma or LPS, also expressed significant amounts
      of DLM-1. Up-regulation of DLM-1 became evident by 4h after stimulation with
      IFN-gamma and was not blocked by cycloheximide, suggesting the presence of IFN
      responding elements in its transcription regulation region. DLM-1 RNA was
      detected at significant levels in normal mouse lung, intestinal epithelium, liver
      and thymus by Northern blot analysis. In situ hybridization of MOT and HT-29
      mouse subcutaneous transplanted solid tumors revealed strong DLM-1 expression in 
      the host reactive stromal cells, but not the tumor cells. Sequence analysis of
      the full-length cDNA clone revealed that it encodes a protein of approx. M(r)
      44330 with multiple potential protein kinase C and casein kinase II
      phosphorylation sites. Our data suggest that DLM-1 plays a role in such important
      processes as host response in neoplasia.
FAU - Fu, Y
AU  - Fu Y
AD  - Department of Pathology, Beth Israel-Deaconess Medical Center and Harvard Medical
      School, Boston, MA, USA. yfu@caregroup.harvard.edu
FAU - Comella, N
AU  - Comella N
FAU - Tognazzi, K
AU  - Tognazzi K
FAU - Brown, L F
AU  - Brown LF
FAU - Dvorak, H F
AU  - Dvorak HF
FAU - Kocher, O
AU  - Kocher O
LA  - eng
SI  - GENBANK/AF136520
GR  - CA-50453/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Gene
JT  - Gene
JID - 7706761
RN  - 0 (Cytokines)
RN  - 0 (DNA, Complementary)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Glycoproteins)
RN  - 0 (Igf2bp1 protein, rat)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Neoplasm)
RN  - 0 (RNA-Binding Proteins)
RN  - 0 (ZBP1 protein, human)
RN  - 0 (Zbp1 protein, mouse)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Blotting, Northern
MH  - Cloning, Molecular
MH  - Cytokines/pharmacology
MH  - DNA, Complementary/chemistry/genetics/isolation & purification
MH  - *DNA-Binding Proteins
MH  - Female
MH  - Gene Expression Regulation/drug effects
MH  - Glycoproteins/*genetics
MH  - Humans
MH  - In Situ Hybridization
MH  - Macrophage Activation/*genetics
MH  - Macrophages, Peritoneal/cytology/drug effects/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Molecular Sequence Data
MH  - Neoplasm Transplantation
MH  - Neoplasms, Experimental/genetics/pathology
MH  - RNA, Messenger/genetics/metabolism
MH  - RNA, Neoplasm/*genetics
MH  - RNA-Binding Proteins
MH  - Sequence Analysis, DNA
MH  - Tissue Distribution
MH  - Tumor Cells, Cultured
MH  - Up-Regulation
EDAT- 1999/11/24 00:00
MHDA- 1999/11/24 00:01
CRDT- 1999/11/24 00:00
PHST- 1999/11/24 00:00 [pubmed]
PHST- 1999/11/24 00:01 [medline]
PHST- 1999/11/24 00:00 [entrez]
AID - S0378-1119(99)00419-9 [pii]
AID - 10.1016/s0378-1119(99)00419-9 [doi]
PST - ppublish
SO  - Gene. 1999 Nov 15;240(1):157-63. doi: 10.1016/s0378-1119(99)00419-9.