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Table representation of search results timeline featuring number of search results per year.

Year Number of Results
1946 1
1947 1
1949 1
1950 4
1954 2
1955 2
1956 3
1957 3
1958 3
1959 3
1960 3
1961 5
1962 2
1963 3
1964 4
1965 5
1966 5
1967 7
1968 10
1969 5
1970 9
1971 8
1972 15
1973 10
1974 8
1975 50
1976 30
1977 30
1978 23
1979 52
1980 31
1981 60
1982 54
1983 84
1984 76
1985 83
1986 92
1987 72
1988 77
1989 113
1990 113
1991 112
1992 128
1993 131
1994 114
1995 164
1996 156
1997 144
1998 184
1999 191
2000 232
2001 495
2002 389
2003 365
2004 406
2005 270
2006 222
2007 211
2008 187
2009 198
2010 215
2011 197
2012 211
2013 158
2014 127
2015 116
2016 97
2017 90
2018 92
2019 60
2020 59
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6,792 results
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Page 1
Withdrawal: Role of extracellular matrix renal tubulo-interstitial nephritis antigen (TINag) in cell survival utilizing integrin alphavbeta3/focal adhesion kinase (FAK)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B-serine/threonine kinase (AKT) signaling pathway.
Xie P, Kondeti VK, Lin S, Haruna Y, Raparia K, Kanwar YS. Xie P, et al. J Biol Chem. 2019 Jun 28;294(26):10379. doi: 10.1074/jbc.W119.009585. J Biol Chem. 2019. PMID: 31253687 Free PMC article. No abstract available.
14-3-3sigma Gene Loss Leads to Activation of the Epithelial to Mesenchymal Transition Due to the Stabilization of c-Jun Protein.
Raychaudhuri K, Chaudhary N, Gurjar M, D'Souza R, Limzerwala J, Maddika S, Dalal SN. Raychaudhuri K, et al. J Biol Chem. 2016 Jul 29;291(31):16068-81. doi: 10.1074/jbc.M116.723767. Epub 2016 Jun 3. J Biol Chem. 2016. PMID: 27261462 Free PMC article.
The EMT was accompanied by an increase in migration and invasion in the 14-3-3sigma(-/-) cells. 14-3-3sigma(-/-) cells show increased stabilization of c-Jun, resulting in an increase in the expression of the EMT transcription factor slug. 14-3-3sigma i …
The EMT was accompanied by an increase in migration and invasion in the 14-3-3sigma(-/-) cells. 14-3-3sigma(-/-) cells show in …
Anthrax lethal toxin rapidly reduces c-Jun levels by inhibiting c-Jun gene transcription and promoting c-Jun protein degradation.
Ouyang W, Guo P, Fang H, Frucht DM. Ouyang W, et al. J Biol Chem. 2017 Oct 27;292(43):17919-17927. doi: 10.1074/jbc.M117.805648. Epub 2017 Sep 11. J Biol Chem. 2017. PMID: 28893904 Free PMC article.
The restoration of c-Jun in U0126-exposed cells was associated with increased c-Jun mRNA levels and was blocked by inactivation of the JNK1/2 signaling pathway. These results indicate that LT reduces c-Jun both by promoting c-Jun protein degradation vi …
The restoration of c-Jun in U0126-exposed cells was associated with increased c-Jun mRNA levels and was blocked by inactivatio …
MEKK2 kinase association with 14-3-3 protein regulates activation of c-Jun N-terminal kinase.
Matitau AE, Gabor TV, Gill RM, Scheid MP. Matitau AE, et al. J Biol Chem. 2013 Sep 27;288(39):28293-302. doi: 10.1074/jbc.M113.511352. Epub 2013 Aug 20. J Biol Chem. 2013. PMID: 23963453 Free PMC article.
Mechanistically, we found that MEKK2 associated with inactive MEKK2 in the absence of 14-3-3 binding, which led to trans-autophosphorylation of Ser-519. Enforced binding with 14-3-3 reduced Ser-519 trans-autophosphorylation. Expression of T283A MEKK2 w …
Mechanistically, we found that MEKK2 associated with inactive MEKK2 in the absence of 14-3-3 binding, which led to trans-autop …
Selective association of protein kinase C with 14-3-3 zeta in neuronally differentiated PC12 Cells. Stimulatory and inhibitory effect of 14-3-3 zeta in vivo.
Gannon-Murakami L, Murakami K. Gannon-Murakami L, et al. J Biol Chem. 2002 Jun 28;277(26):23116-22. doi: 10.1074/jbc.M201478200. Epub 2002 Apr 11. J Biol Chem. 2002. PMID: 11950841 Free article.
Although 14-3-3 zeta was originally characterized as an endogenous PKC inhibitor, it was reported to activate PKC in vitro, but the in vivo regulation of PKC by 14-3-3 is still not well understood. To examine the regulation of PKC by 14-3-3
Although 14-3-3 zeta was originally characterized as an endogenous PKC inhibitor, it was reported to activate PKC in vitro, bu …
Stress-induced c-Jun-dependent Vitamin D receptor (VDR) activation dissects the non-classical VDR pathway from the classical VDR activity.
Li QP, Qi X, Pramanik R, Pohl NM, Loesch M, Chen G. Li QP, et al. J Biol Chem. 2007 Jan 19;282(3):1544-51. doi: 10.1074/jbc.M604052200. Epub 2006 Nov 22. J Biol Chem. 2007. PMID: 17121851 Free article.
The necessary and sufficient role of c-Jun in VDR expression was established by the fact that c-Jun knock-out decreases VDR expression, whereas c-Jun restoration recovers its activity. Existence of the non-classical VDR pathway was suggested by a requirement …
The necessary and sufficient role of c-Jun in VDR expression was established by the fact that c-Jun knock-out decreases VDR ex …
c-Jun N-terminal kinase 3 deficiency protects neurons from axotomy-induced death in vivo through mechanisms independent of c-Jun phosphorylation.
Keramaris E, Vanderluit JL, Bahadori M, Mousavi K, Davis RJ, Flavell R, Slack RS, Park DS. Keramaris E, et al. J Biol Chem. 2005 Jan 14;280(2):1132-41. doi: 10.1074/jbc.M410127200. Epub 2004 Nov 4. J Biol Chem. 2005. PMID: 15528206 Free article.
Both the transcription factor c-Jun and the c-Jun N-terminal kinases (JNKs) have been associated with neuronal loss in several death paradigms. ...JNK2 and JNK2/3 double-deficient animals also showed reduced c-Jun phosphorylation and induction followin …
Both the transcription factor c-Jun and the c-Jun N-terminal kinases (JNKs) have been associated with neuronal loss in several …
Structural characterization of the primary O-antigenic polysaccharide of the Rhizobium leguminosarum 3841 lipopolysaccharide and identification of a new 3-acetimidoylamino-3-deoxyhexuronic acid glycosyl component: a unique O-methylated glycan of uniform size, containing 6-deoxy-3-O-methyl-D-talose, n-acetylquinovosamine, and rhizoaminuronic acid (3-acetimidoylamino-3-deoxy-D-gluco-hexuronic acid).
Forsberg LS, Carlson RW. Forsberg LS, et al. J Biol Chem. 2008 Jun 6;283(23):16037-50. doi: 10.1074/jbc.M709615200. Epub 2008 Apr 2. J Biol Chem. 2008. PMID: 18387959 Free PMC article.
The OPS is composed of several unusual glycosyl residues, including 6-deoxy-3-O-methyl-d-talose and 2-acetamido-2deoxy-l-quinovosamine. In addition, a new glycosyl residue, 3-acetimidoylamino-3-deoxy-d-gluco-hexuronic acid was identified and characterized, a …
The OPS is composed of several unusual glycosyl residues, including 6-deoxy-3-O-methyl-d-talose and 2-acetamido-2deoxy-l-quinovosamin …
Enhancement of interleukin-3-dependent mast cell proliferation by suppression of c-jun expression.
Chaikin E, Hakeem I, Razin E. Chaikin E, et al. J Biol Chem. 1994 Mar 18;269(11):8498-503. J Biol Chem. 1994. PMID: 8132577 Free article.
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
We have previously shown that protein kinase C (PKC) depletion is associated with an increase in the proliferation of interleukin 3 ( …
The 3'-azido group is not the primary determinant of 3'-azido-3'-deoxythymidine (AZT) responsible for the excision phenotype of AZT-resistant HIV-1.
Sluis-Cremer N, Arion D, Parikh U, Koontz D, Schinazi RF, Mellors JW, Parniak MA. Sluis-Cremer N, et al. J Biol Chem. 2005 Aug 12;280(32):29047-52. doi: 10.1074/jbc.M503166200. Epub 2005 Jun 20. J Biol Chem. 2005. PMID: 15970587 Free article.
Primers terminated with AZTMP are generally better substrates for this reaction than those terminated with 2',3'-dideoxynucleoside-5'-monophosphate (2',3'-ddNMP) analogs that lack a 3'-azido moiety. ...To test this hypothesis, we evaluated the incorporation, …
Primers terminated with AZTMP are generally better substrates for this reaction than those terminated with 2',3'-dideoxynucleoside-5' …
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