PMID- 8547646
OWN - NLM
STAT- MEDLINE
DCOM- 19960216
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 87
IP  - 1
DP  - 1996 Jan 1
TI  - Myeloid differentiation and retinoblastoma phosphorylation changes in HL-60 cells 
      induced by retinoic acid receptor- and retinoid X receptor-selective retinoic 
      acid analogs.
PG  - 227-37
AB  - The ability of subtypes of retinoic acid receptors (RARs) and retinoid X 
      receptors (RXRs) singly and in combination to elicit myeloid differentiation, 
      G1/0-specific growth arrest, and retinoblastoma (RB) tumor suppressor protein 
      dephosphorylation was determined in the human myeloblastic leukemia cell line 
      HL-60 using subtype-selective retinoic acid (RA) analogs. RA analogs that 
      selectively bind only to RARs (Am580 and/or TTNPB) or to RXRs (Ro 25-6603, 
      SR11237, and/or SR11234) did not elicit the above-mentioned three cellular 
      responses. In contrast, simultaneous treatment with both an RAR-selective ligand 
      (Am580 or TTNPB) and an RXR-selective ligand (Ro 25-6603, SR11237, or SR11234) 
      induced all three cellular processes. An RAR alpha-selective ligand used with an 
      RXR-selective ligand generated the same responses as did all-trans RA or 9-cis 
      RA, which affect both families of receptors, suggesting an important role for RAR 
      alpha among RAR subtypes in eliciting cellular response. Consistent with this 
      finding, the RAR alpha antagonist, Ro 41-5253, reduced the level of the cellular 
      responses elicited by treatment with an RAR alpha-selective ligand plus 
      RXR-selective ligand. The coupling of the shift of RB to its hypophosphorylated 
      form with G1/0 arrest and differentiation in response to ligands is consistent 
      with a possible role of RB as a downstream target or effector of RAR alpha and 
      RXR in combination.
FAU - Brooks, S C 3rd
AU  - Brooks SC 3rd
AD  - Department of Pathology, Cornell University, Ithaca, NY 14853, USA.
FAU - Kazmer, S
AU  - Kazmer S
FAU - Levin, A A
AU  - Levin AA
FAU - Yen, A
AU  - Yen A
LA  - eng
GR  - ES 07052/ES/NIEHS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Benzoates)
RN  - 0 (Chromans)
RN  - 0 (Cyclohexanes)
RN  - 0 (Fatty Acids, Unsaturated)
RN  - 0 (Ligands)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Pentanoic Acids)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoblastoma Protein)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Retinoids)
RN  - 0 (Ro 25-5802)
RN  - 0 (Ro 25-6603)
RN  - 0 (Tetrahydronaphthalenes)
RN  - 0 (Transcription Factors)
RN  - 102121-60-8 (Am 580)
RN  - 144092-31-9 (Ro 41-5253)
RN  - 146670-37-3 (SR 11234)
RN  - 146670-40-8 (SR 11237)
RN  - 5688UTC01R (Tretinoin)
RN  - 71441-28-6 
      (4-(2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1-propenyl)benzoic 
      acid)
SB  - IM
MH  - *Benzoates/pharmacology
MH  - Cell Differentiation/drug effects
MH  - Chromans/pharmacology
MH  - Cyclohexanes/pharmacology
MH  - Fatty Acids, Unsaturated/pharmacology
MH  - Flow Cytometry
MH  - HL-60 Cells/*drug effects/metabolism
MH  - Humans
MH  - Ligands
MH  - Neoplasm Proteins/*metabolism
MH  - Pentanoic Acids/pharmacology
MH  - Phosphorylation/drug effects
MH  - Protein Processing, Post-Translational/*drug effects
MH  - Receptors, Retinoic Acid/*drug effects/physiology
MH  - Retinoblastoma Protein/*metabolism
MH  - Retinoid X Receptors
MH  - Retinoids/pharmacology
MH  - Structure-Activity Relationship
MH  - Substrate Specificity
MH  - Tetrahydronaphthalenes/pharmacology
MH  - Transcription Factors/*drug effects/physiology
MH  - Tretinoin/*analogs & derivatives/pharmacology
EDAT- 1996/01/01 00:00
MHDA- 2001/03/28 10:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - S0006-4971(20)66212-7 [pii]
PST - ppublish
SO  - Blood. 1996 Jan 1;87(1):227-37.