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Axl (human)

Overview Axl a receptor tyrosine kinase that may function as a signal transducer between specific cell types of mesodermal origin. Interacts with SKP1. Overexpression in tissue culture causes oncogenic transformation. Overexpressed in several cancers including thyroid, ovarian, gastric, ER+ breast cancer and acute myeloid leukemia, where it is associated with poor prognosis. 2 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB. Protein type: Protein kinase, TK; Membrane protein, integral; Kinase, protein; Protein kinase, tyrosine (receptor); EC 2.7.10.1; TK group; Axl family Cellular Component: extracellular space; cell surface; integral to plasma membrane Molecular Function: protein binding; protein heterodimerization activity; phosphatidylserine binding; transmembrane receptor protein tyrosine kinase activity; ATP binding Biological Process: cell maturation; neuron migration; signal transduction; enzyme linked receptor protein signaling pathway; positive regulation of natural killer cell differentiation; erythrocyte homeostasis; ovulation cycle; natural killer cell differentiation; negative regulation of interferon-gamma production; protein kinase B signaling cascade; negative regulation of neuron apoptosis; inflammatory response; secretion by cell; forebrain cell migration; negative regulation of lymphocyte activation; platelet activation; vagina development; negative regulation of tumor necrosis factor production; phagocytosis; positive regulation of protein kinase B signaling cascade; cellular response to extracellular stimulus; innate immune response; spermatogenesis; blood vessel remodeling; positive regulation of cytokine and chemokine mediated signaling pathway; apoptotic cell clearance Reference #:  P30530 (UniProtKB) Alt. Names/Synonyms: AXL; AXL oncogene; AXL receptor tyrosine kinase; AXL transforming sequence/gene; JTK11; oncogene AXL; Tyrosine-protein kinase receptor UFO; UFO Gene Symbols: AXL Molecular weight: 98,336 Da Basal Isoelectric point: 5.27  Predict pI for various phosphorylation states CST Pathways:  Tyrosine Kinases Protein-Specific Antibodies or siRNAs from Cell Signaling Technology®

Select Structure to View Below Axl 2C5D - C/D=26-220 (human)

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	Sites Implicated In
molecular association, regulation: Y821‑p

	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		S100-p	QDDWIVVsQLRITSL
0	1		S110	RITSLQLSDTGQYQC
0	1		Y115	QLSDTGQYQCLVFLG
0	1		T200-p	HVPGLNKtssFsCEA
0	1		S201-p	VPGLNKtssFsCEAH
0	1		S202-p	PGLNKtssFsCEAHN
0	1		S204-p	LNKtssFsCEAHNAK
0	1		T256	LSGIYPLTHCTLQAV
0	1		S265	CTLQAVLSNDGMGIQ
0	4		Y481-p	RRKKETRyGEVFEPT
0	1		S503-p	VRYRVRKsYSRRttE
0	1		T508-p	RKsYSRRttEATLNs
0	2		T509-p	KsYSRRttEATLNsL
0	1		S515-p	ttEATLNsLGISEEL
0	3		K523-u	LGISEELkEKLRDVM
0	8		K540-u	RHKVALGkTLGEGEF
0	1		K563-u	NQDDSILkVAVKTMK
0	1		K570	kVAVKTMKIAICTRS
0	1		S612-p	FQGSEREsFPAPVVI
0	3		Y634-p	DLHSFLLySRLGDQP
0	1		S635	LHSFLLySRLGDQPV
0	1		Y643-p	RLGDQPVyLPTQMLV
0	1		T646	DQPVyLPTQMLVKFM
0	1		K666-u	GMEYLSTkRFIHRDL
0	54		Y698-p	FGLSKKIyNGDyyRQ
0	764		Y702-p	KKIyNGDyyRQGRIA
0	362		Y703-p	KIyNGDyyRQGRIAK
0	6		R724-m2	AIESLADrVyTSKSD
0	2		Y726-p	ESLADrVyTSKSDVW
0	12		Y759-p	GVENSEIyDyLRQGN
0	1		Y761-p	ENSEIyDyLRQGNRL
0	1		K769	LRQGNRLKQPADCLD
0	2		Y779-p	ADCLDGLyALMSRCW
1	1		Y821-p	QEPDEILyVNMDEGG
1	13		Y866-p	EVHPAGRyVLCPSTT
0	1		S875-p	LCPSTTPsPAQPADR
0	1		S884-p	AQPADRGsPAAPGQE

	mouse
S94	QDEWKVVSQLRISAL
S104-p	RISALQLsDAGEyQC
Y109-p	QLsDAGEyQCMVHLE
T194	QTPGLNKTSSFSCEA
S195	TPGLNKTSSFSCEAH
S196	PGLNKTSSFSCEAHN
S198	LNKTSSFSCEAHNAK
T250-p	LSGIYPLtHCNLQAV
S259-p	CNLQAVLsDDGVGIW
Y475-p	RRKKETRyGEVFEPT
S497	VRYRVRKSYSRRttE
T502-p	RKSYSRRttEATLNs
T503-p	KSYSRRttEATLNsL
S509-p	ttEATLNsLGISEEL
K517-u	LGISEELkEKLRDVM
K534-u	RHKVALGkTLGEGEF
K557	NQDDSILKVAVKTMk
K564-u	KVAVKTMkIAICTRS
G606	FQGSDREGFPEPVVI
Y628	DLHSFLLYsRLGDQP
S629-p	LHSFLLYsRLGDQPV
F637	RLGDQPVFLPtQMLV
T640-p	DQPVFLPtQMLVKFM
K660	GMEYLSTKRFIHRDL
Y692-p	FGLSKKIyNGDyyRQ
Y696-p	KKIyNGDyyRQGRIA
Y697-p	KIyNGDyyRQGRIAK
R718	AIESLADRVYTSKSD
Y720	ESLADRVYTSKSDVW
Y753	GVENSEIYDyLRQGN
Y755-p	ENSEIYDyLRQGNRL
K763-u	LRQGNRLkQPVDCLD
Y773	VDCLDGLYALMSRCW
Y815-p	QEPDEILyVNMDEGG
Y860-p	DVHSAGRyVLCPSTA
G869	LCPSTAPGPTLSADR
C878	TLSADRGCPAPPGQE

	rat
S94	QDEWKVVSQLRISAL
S104	RISALQLSDAGEYQC
Y109	QLSDAGEYQCMVHLE
T194	QAPGLNKTSSFSCEA
S195	APGLNKTSSFSCEAH
S196	PGLNKTSSFSCEAHN
S198	LNKTSSFSCEAHNAK
T250	LSGIYPLTHCTLQAV
S259	CTLQAVLSNDGVGVW
Y475-p	RRKKETRyGEVFEPT
S497	VRYRARKSYSRRTtE
T502	RKSYSRRTtEATLNS
T503-p	KSYSRRTtEATLNSL
S509	TtEATLNSLGISEEL
K517	LGISEELKEKLRDVM
K534	RHKVALGKTLGEGEF
K557	NQDDSILKVAVKTMK
K564	KVAVKTMKIAICTRS
G606	FQGSDREGFPEPVVI
Y628	DLHSFLLYSRLGDQP
S629	LHSFLLYSRLGDQPV
F637	RLGDQPVFLPTQMLV
T640	DQPVFLPTQMLVKFM
K660	GMEYLSTKRFIHRDL
Y692-p	FGLSKKIyNGDyyRQ
Y696-p	KKIyNGDyyRQGRIA
Y697-p	KIyNGDyyRQGRIAK
R718	AIESLADRVYTSKSD
Y720	ESLADRVYTSKSDVW
Y753	GVENSEIYDYLRQGN
Y755	ENSEIYDYLRQGNRL
K763	LRQGNRLKQPLDCLD
Y773	LDCLDGLYALMSRCW
Y815	QEPDEILYVNMDEGG
Y860	DVHSAGRYVLCPSTA
G869	LCPSTAPGPTLSADR
C878	TLSADRGCPAPPGQE

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