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GNL3 (human)

Overview GNL3 May be required to maintain the proliferative capacity of stem cells and may play an important role in tumorigenesis. May interact with p53/TP53 via its basic domain. Increased levels in lung tissue in cancer patients. Belongs to the MMR1/HSR1 GTP-binding protein family. 2 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB. Protein type: Hydrolase; Cell cycle regulation Cellular Component: nucleoplasm; nucleolus; nucleus Molecular Function: GTPase activity; protein binding; GTP binding Biological Process: cell proliferation; GTP catabolic process; ribosome biogenesis and assembly; regulation of cell proliferation Reference #:  Q9BVP2 (UniProtKB) Alt. Names/Synonyms: C77032; E2-induced gene 3 protein; E2IG3; estradiol-induced nucleotide binding protein; GNL3; guanine nucleotide binding protein-like 3 (nucleolar); Guanine nucleotide-binding protein-like 3; MGC800; NNP47; Novel nucleolar protein 47; NS; Nucleolar GTP-binding protein 3; Nucleostemin Gene Symbols: GNL3 Molecular weight: 61,993 Da Basal Isoelectric point: 9.23  Predict pI for various phosphorylation states Protein-Specific Antibodies or siRNAs from Cell Signaling Technology®

Select Structure to View Below GNL3

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	Modification Sites and Domains	Show Modification Legend
Click here to view phosphorylation modifications only

	Modification Sites in Parent Protein, Orthologs, and Isoforms	Show Modification Legend

SS  SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.	MS  MS: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.			human
0	1		K5-a	___MKRPkLKKASKR
0	3		K17-a	SKRMTCHkRYKIQKK
0	1		K79-a	EELKQQQkLDRQKEL
0	8		N95	KKRKLETNPDIKPSN
0	1		K171-u	AIVQSGQkKLVLILN
1	1		Y194-p	NLESWLNyLkkELPT
0	2		K196-u	ESWLNyLkkELPTVV
0	2		K197-u	SWLNyLkkELPTVVF
0	1		K237-a	RSEVCFGkEGLWkLL
0	7		K237-u	RSEVCFGkEGLWkLL
0	1		K242-u	FGkEGLWkLLGGFQE
0	11		K253-u	GFQETCSkAIRVGVI
0	3		K267-u	IGFPNVGkSSIINsL
0	1		S273-p	GkSSIINsLkQEQMC
0	1		K275-u	SSIINsLkQEQMCNV
0	1		T289-p	VGVSMGLtRSMQVVP
0	3		K332-u	PASIEVVkPMEAASA
0	1		T366-p	RNSLEFFtVLAQRRG
0	1		K377-u	QRRGMHQkGGIPNVE
0	1		K444-u	AQSIRAIkGPHLANS
0	1		L473	EKDIHEELPKRKERK
0	2		S490-p	EREDDKDsDQETVDE
0	1		S503-p	DEEVDENsSGMFAAE
0	3		S504	EEVDENsSGMFAAEE
0	2		T512	GMFAAEETGEALSEE
0	21		L516	AEETGEALSEETTAG
0	1		T520	GEALSEETTAGEQST
0	2		S529-p	AGEQSTRsFILDKII
0	14		Y542-p	IIEEDDAyDFsTDyV
0	2		S545-p	EDDAyDFsTDyV___
0	8		Y548-p	AyDFsTDyV______

	mouse
K5	___MKRPKLKKASKR
K17	SKRMTCHKRYKIQKK
K79	EELKQQQKLDRQKEQ
S95-p	RKRKLEVsPGDEQSN
K169	AVIQSGSKKLILVLN
Y192	NLENWLNYLNKELPT
N194	ENWLNYLNKELPTVV
K195	NWLNYLNKELPTVVF
K232	QSKICCGKEALWKLL
K232	QSKICCGKEALWKLL
K237	CGKEALWKLLGDFQQ
K248	DFQQSCGKDIQVGVI
K262	IGFPNVGKSSVINSL
S268	GKSSVINSLKQEWIC
K270	SSVINSLKQEWICNV
T284	VGISMGLTRSMQIVP
R327	PASIEELRPLEAASA
T361	KDSLHFFTKLAQRRG
K372	QRRGLHQKGGSPNVE
K439	AHSIQVLKGPHLTNR
S468-p	EKDIVEEsPRQTEDK
-	gap
-	under review
S493-p	GERNAEIsDVAPVEE
T501-p	DVAPVEEtRELsPEQ
S505-p	VEEtRELsPEQsTAG
S509-p	RELsPEQsTAGKPSD
S518	AGKPSDGSSALDRAS
Y531	ASQEDETYDFTTDYI
T534	EDETYDFTTDYI___
Y537	TYDFTTDYI______

	rat
K5	___MKRPKLKKASKR
K17	SKRMTCHKRYKIQKK
K79	EELKQQQKLDRQKEQ
S95	RKRKLEISPDDEQSN
K169	AVIQSGCKKLVLVLN
Y192	NLENWLTYLNKELPT
N194	ENWLTYLNKELPTVV
K195	NWLTYLNKELPTVVF
K232	QSKLCCGKEALWKLL
K232	QSKLCCGKEALWKLL
K237	CGKEALWKLLGGFQQ
K248	GFQQSCGKGVQVGVV
K262	VGFPNVGKSSIINSL
S268	GKSSIINSLKQERIC
K270	SSIINSLKQERICSV
T284	VGVSMGLTRSMQIVP
R327	PASIEVLRPLEAASA
T361	KDSLDFFTKLAQRRG
K372	QRRGLHQKGGSPNVE
K439	AHSIQVLKGPHLTNK
S468	EKDIPEESPKQTEDQ
-	under review
-	under review
S493	GEKNAEISDVTPVEE
T501	DVTPVEETREMSPGQ
S505	VEETREMSPGQSTAS
S509	REMSPGQSTASKPSD
S518	ASKPSDRSFILDKMS
Y531	MSEEDDAYDFTTDYI
T534	EDDAYDFTTDYI___
Y537	AYDFTTDYI______

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