NDLI: Enhancement of interleukin-3-dependent mast cell proliferation by suppression of c-jun expression.

Content Provider	Journal of Biological Chemistry (JBC)
Author	Chaikin, E. Hakeem, I. Razin, E.
Abstract	We have previously shown that protein kinase C (PKC) depletion is associated with an increase in the proliferation of interleukin 3 (IL-3)-induced mast cells. Here we show that the AP-1 components c-Jun and c-Fos are induced by IL-3. While c-Jun's induction by IL-3 is totally dependent on PKC, c-Fos induction by IL-3 is only attenuated by PKC depletion. AP-1 binding activity was also induced by IL-3 but this induction was PKC independent. These results indicated a possible involvement of c-Jun in the inhibition of IL-3-induced growth regulation. A support for this assumption came from experiments in which an increase in thymidine incorporation into mast cells was noted when c-jun antisense oligomers were administered to IL-3-treated cells. Since the only known effect of direct inhibition of c-Jun on proliferation rates in several cellular systems was a reduction of proliferation, we verified that our c-jun antisense oligomer could also inhibit proliferation rates in fibroblasts where such a repression was previously reported. Thus c-Jun has an inhibitory effect on IL-3 induction of mast cells proliferation that is distinct from its role in several other cellular environments. These observations reveal the involvement of AP-1 and its components in IL-3-induced signal transduction and the importance of the mast cell environment in determining their specific cellular function.
Related Links	http://www.jbc.org/content/269/11/8498.abstract
Ending Page	8503
Starting Page	8498
Page Count	6
File Format	HTM / HTML PDF
ISSN	00219258
Journal	Journal of Biological Chemistry (JBC)
Issue Number	11
Volume Number	269
e-ISSN	1083351X
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	1994-03-18
Access Restriction	Open
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Protein kinase C plays an inhibitory role in interleukin 3- and interleukin 4-mediated mast cell proliferation.

Tumor suppression involves down-regulation of interleukin 3 expression in hybrids between autocrine mastocytoma and interleukin 3-dependent parental mast cells.

MEKK2 Kinase Association with 14-3-3 Protein Regulates Activation of c-Jun N-terminal Kinase

Mast cell chymase promotes cell proliferation and expression of certain cytokines in a dose-dependent manner.

Mouse heparin proteoglycan. Synthesis by mast cell-fibroblast monolayers during lymphocyte-dependent mast cell proliferation.

c-Jun Enhancement of Cyclic Adenosine 3′,5′-Monophosphate Response Element-Dependent Transcription Induced by Transforming Growth Factor-β Is Independent of c-Jun Binding to DNA

Ras-dependent Activation of c-Jun N-terminal Kinase/Stress-activated Protein Kinase in Response to Interleukin-3 Stimulation in Hematopoietic BaF3 Cells

Suppression of interleukin-3-induced gene expression by a C-terminal truncated Stat5: role of Stat5 in proliferation.

Anthrax lethal toxin rapidly reduces c-Jun levels by inhibiting c-Jun gene transcription and promoting c-Jun protein degradation

Enhancement of interleukin-3-dependent mast cell proliferation by suppression of c-jun expression.

Similar Documents

Protein kinase C plays an inhibitory role in interleukin 3- and interleukin 4-mediated mast cell proliferation.

Tumor suppression involves down-regulation of interleukin 3 expression in hybrids between autocrine mastocytoma and interleukin 3-dependent parental mast cells.

MEKK2 Kinase Association with 14-3-3 Protein Regulates Activation of c-Jun N-terminal Kinase

Mast cell chymase promotes cell proliferation and expression of certain cytokines in a dose-dependent manner.

Mouse heparin proteoglycan. Synthesis by mast cell-fibroblast monolayers during lymphocyte-dependent mast cell proliferation.

c-Jun Enhancement of Cyclic Adenosine 3′,5′-Monophosphate Response Element-Dependent Transcription Induced by Transforming Growth Factor-β Is Independent of c-Jun Binding to DNA

Ras-dependent Activation of c-Jun N-terminal Kinase/Stress-activated Protein Kinase in Response to Interleukin-3 Stimulation in Hematopoietic BaF3 Cells

Suppression of interleukin-3-induced gene expression by a C-terminal truncated Stat5: role of Stat5 in proliferation.

Anthrax lethal toxin rapidly reduces c-Jun levels by inhibiting c-Jun gene transcription and promoting c-Jun protein degradation

Enhancement of interleukin-3-dependent mast cell proliferation by suppression of c-jun expression.