CREB3L1

CAMP responsive element binding protein 3 like 1 is a responsive element binding protein that in humans is encoded by the CREB3L1 gene.[4]

CREB3L1
Identifiers
Aliases	CREB3L1, OASIS, cAMP responsive element binding protein 3-like 1, cAMP responsive element binding protein 3 like 1, OI16
External IDs	OMIM: 616215 MGI: 1347062 HomoloGene: 8058 GeneCards: CREB3L1
Gene location (Human) Chr. Chromosome 11 (human)[1] Band 11p11.2 Start 46,277,662 bp[1] End 46,321,409 bp[1]
Gene ontology Molecular function • DNA binding • GO:0001131, GO:0001151, GO:0001130, GO:0001204 DNA-binding transcription factor activity • GO:0001077, GO:0001212, GO:0001213, GO:0001211, GO:0001205 DNA-binding transcription activator activity, RNA polymerase II-specific • chromatin binding • GO:0001948 protein binding • cAMP response element binding • SMAD binding • GO:0001200, GO:0001133, GO:0001201 DNA-binding transcription factor activity, RNA polymerase II-specific • GO:0001078, GO:0001214, GO:0001206 DNA-binding transcription repressor activity, RNA polymerase II-specific Cellular component • integral component of membrane • endoplasmic reticulum membrane • endoplasmic reticulum • cell nucleus • membrane • nuclear chromatin Biological process • negative regulation of endoplasmic reticulum stress-induced intrinsic apoptotic signaling pathway • regulation of transcription, DNA-templated • extracellular matrix constituent secretion • positive regulation of transcription from RNA polymerase II promoter in response to endoplasmic reticulum stress • transcription, DNA-templated • multicellular organism development • endoplasmic reticulum unfolded protein response • response to unfolded protein • osteoblast differentiation • positive regulation of transcription from RNA polymerase II promoter • transcription from RNA polymerase II promoter • positive regulation of collagen biosynthetic process • negative regulation of transcription from RNA polymerase II promoter • negative regulation of gene expression • negative regulation of fibroblast growth factor receptor signaling pathway • negative regulation of transcription, DNA-templated • negative regulation of sprouting angiogenesis Sources:Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	90993	26427
Ensembl	ENSG00000157613	n/a
UniProt	Q96BA8	Q9Z125
RefSeq (mRNA)	NM_052854	NM_011957
RefSeq (protein)	NP_443086	NP_036087
Location (UCSC)	Chr 11: 46.28 – 46.32 Mb	n/a
PubMed search	[2]	[3]
Wikidata
View/Edit Human View/Edit Mouse

Function

The protein encoded by this gene is normally found in the membrane of the endoplasmic reticulum (ER). However, upon stress to the ER, the encoded protein is cleaved, and the released cytoplasmic transcription factor domain translocates to the nucleus. There it activates the transcription of target genes by binding to box-B elements. [provided by RefSeq, Jun 2013].

References

1. GRCh38: Ensembl release 89: ENSG00000157613 - Ensembl, May 2017
2. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
3. "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
4. "Entrez Gene: CAMP responsive element binding protein 3 like 1".

Further reading

• Omori Y, Imai J, Suzuki Y, Watanabe S, Tanigami A, Sugano S (April 2002). "OASIS is a transcriptional activator of CREB/ATF family with a transmembrane domain". Biochemical and Biophysical Research Communications. 293 (1): 470–7. doi:10.1016/S0006-291X(02)00253-X. PMID 12054625.
• Guillou L, Benhattar J, Gengler C, Gallagher G, Ranchère-Vince D, Collin F, Terrier P, Terrier-Lacombe MJ, Leroux A, Marquès B, Aubain Somerhausen N, Keslair F, Pedeutour F, Coindre JM (September 2007). "Translocation-positive low-grade fibromyxoid sarcoma: clinicopathologic and molecular analysis of a series expanding the morphologic spectrum and suggesting potential relationship to sclerosing epithelioid fibrosarcoma: a study from the French Sarcoma Group". The American Journal of Surgical Pathology. 31 (9): 1387–402. doi:10.1097/PAS.0b013e3180321959. PMID 17721195.
• Fox RM, Hanlon CD, Andrew DJ (November 2010). "The CrebA/Creb3-like transcription factors are major and direct regulators of secretory capacity". The Journal of Cell Biology. 191 (3): 479–92. doi:10.1083/jcb.201004062. PMC 3003312. PMID 21041443.
• Möller E, Hornick JL, Magnusson L, Veerla S, Domanski HA, Mertens F (May 2011). "FUS-CREB3L2/L1-positive sarcomas show a specific gene expression profile with upregulation of CD24 and FOXL1". Clinical Cancer Research. 17 (9): 2646–56. doi:10.1158/1078-0432.CCR-11-0145. PMID 21536545.
• Denard B, Seemann J, Chen Q, Gay A, Huang H, Chen Y, Ye J (July 2011). "The membrane-bound transcription factor CREB3L1 is activated in response to virus infection to inhibit proliferation of virus-infected cells". Cell Host & Microbe. 10 (1): 65–74. doi:10.1016/j.chom.2011.06.006. PMC 3139916. PMID 21767813.
• Denard B, Seemann J, Chen Q, Gay A, Huang H, Chen Y, Ye J (July 2011). "The membrane-bound transcription factor CREB3L1 is activated in response to virus infection to inhibit proliferation of virus-infected cells". Cell Host & Microbe. 10 (1): 65–74. doi:10.1016/j.chom.2011.06.006. PMC 3139916. PMID 21767813.
• Debelenko LV, McGregor LM, Shivakumar BR, Dorfman HD, Raimondi SC (December 2011). "A novel EWSR1-CREB3L1 fusion transcript in a case of small cell osteosarcoma". Genes, Chromosomes & Cancer. 50 (12): 1054–62. doi:10.1002/gcc.20923. PMID 21987447.
• Kondo S, Hino SI, Saito A, Kanemoto S, Kawasaki N, Asada R, Izumi S, Iwamoto H, Oki M, Miyagi H, Kaneko M, Nomura Y, Urano F, Imaizumi K (December 2012). "Activation of OASIS family, ER stress transducers, is dependent on its stabilization". Cell Death and Differentiation. 19 (12): 1939–49. doi:10.1038/cdd.2012.77. PMC 3504707. PMID 22705851.
• Denard B, Lee C, Ye J (December 2012). "Doxorubicin blocks proliferation of cancer cells through proteolytic activation of CREB3L1". eLife. 1: e00090. doi:10.7554/eLife.00090. PMC 3524649. PMID 23256041.

This article incorporates text from the United States National Library of Medicine, which is in the public domain.