PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29391601-5	2018	Mechanistically, we show that Lyn-dependent tyrosine phosphorylation of Bim increases its interaction with anti-apoptotic members such as Bcl-xL, therefore limiting mitochondrial outer membrane permeabilization and subsequent apoptosis.	Tyrosine	44-52	BCL2 like 1	Homo sapiens	138-144	
31606346-4	2019	Herein, we report our development of the first covalent inhibitors of the antiapoptotic protein B-cell lymphoma extra-large (Bcl-xL), utilizing a sulfonyl fluoride (SF) warhead to selectively covalently modify tyrosine 101 of the BH3 domain-binding groove.	Tyrosine	210-218	BCL2 like 1	Homo sapiens	96-123	
31606346-4	2019	Herein, we report our development of the first covalent inhibitors of the antiapoptotic protein B-cell lymphoma extra-large (Bcl-xL), utilizing a sulfonyl fluoride (SF) warhead to selectively covalently modify tyrosine 101 of the BH3 domain-binding groove.	Tyrosine	210-218	BCL2 like 1	Homo sapiens	125-131	
22787435-9	2012	Strikingly, disrupting the tyrosine phosphorylation of SOCS-1 or SOCS-3 impaired the expression of Bcl-X(L) protein and sensitized K562 leukemic cells to undergo apoptosis.	Tyrosine	27-35	BCL2 like 1	Homo sapiens	99-107	
25092868-3	2014	Syk binds robustly to nucleolin and phosphorylates it on tyrosine, enhancing its ability to bind the Bcl-x(L) mRNA.	Tyrosine	57-65	BCL2 like 1	Homo sapiens	101-109	
26712279-1	2016	The OCtamer REpeat (OCRE) has been annotated as a 42-residue sequence motif with 12 tyrosine residues in the spliceosome trans-regulatory elements RBM5 and RBM10 (RBM [RNA-binding motif]), which are known to regulate alternative splicing of Fas and Bcl-x pre-mRNA transcripts.	Tyrosine	84-92	BCL2 like 1	Homo sapiens	249-254	
11714801-5	2001	IL-4 does not promote translocation of Aiolos or Bcl-xL, but induces tyrosine phosphorylation of Aiolos, which is required for dissociation from Bcl-xL.	Tyrosine	69-77	BCL2 like 1	Homo sapiens	145-151	
19597709-1	2010	The present study aims to investigate the mechanism of phosphorylation of apoptotic proteins and tests the hypothesis that the hypoxia-induced increased tyrosine phosphorylation of apoptotic proteins Bcl-2 and Bcl-xl is Ca(2+)-influx-dependent.	Tyrosine	153-161	BCL2 like 1	Homo sapiens	210-216	
16651438-4	2006	Consistent with the increased Fas/CD95 expression, a drastic decrease in the Tyr(705) phosphorylation of STAT3, a known negative regulator of Fas/CD95 transcription, was found within 20 minutes in the luteolin-treated cells, leading to down-regulation in the target gene products of STAT3, such as cyclin D1, survivin, Bcl-xL, and vascular endothelial growth factor.	Tyrosine	77-80	BCL2 like 1	Homo sapiens	319-325	
12411057-5	2002	Tyrosine phosphorylation level of P210(BCR/ABL) and Bcl-X(L) was decreased.	Tyrosine	0-8	BCL2 like 1	Homo sapiens	52-60	
22433870-0	2012	Tyrosine-phosphorylated caveolin-1 (Tyr-14) increases sensitivity to paclitaxel by inhibiting BCL2 and BCLxL proteins via c-Jun N-terminal kinase (JNK).	Tyrosine	0-8	BCL2 like 1	Homo sapiens	103-108	
22433870-0	2012	Tyrosine-phosphorylated caveolin-1 (Tyr-14) increases sensitivity to paclitaxel by inhibiting BCL2 and BCLxL proteins via c-Jun N-terminal kinase (JNK).	Tyrosine	0-3	BCL2 like 1	Homo sapiens	103-108	
20213344-1	2010	The present study tests the hypothesis that hyperoxia results in increased tyrosine phosphorylation of apoptotic proteins Bcl-2, Bcl-xl, Bax & Bad in the mitochondrial fraction of the cerebral cortex of newborn piglets.	Tyrosine	75-83	BCL2 like 1	Homo sapiens	129-135	
20213344-7	2010	The data show that during hyperoxia there is a significant increase in tyrosine phosphorylation of Bcl2 and Bcl-xl, while the phosphorylation of proapototic proteins Bax & Bad was not altered.	Tyrosine	71-79	BCL2 like 1	Homo sapiens	108-114	
20004564-7	2010	The bcl-X(L) was accompanied with a robust increase of Etk and tyrosine phosphorylated Etk at Tyr-40 in H69AR cells.	Tyrosine	63-71	BCL2 like 1	Homo sapiens	4-12	
20004564-7	2010	The bcl-X(L) was accompanied with a robust increase of Etk and tyrosine phosphorylated Etk at Tyr-40 in H69AR cells.	Tyrosine	94-97	BCL2 like 1	Homo sapiens	4-12	
20004564-8	2010	In conclusion, our results suggest that non-receptor tyrosine kinase Etk is involved in drug resistance to SCLC by mediating bcl-X(L) via Tyr(P)-40.	Tyrosine	138-141	BCL2 like 1	Homo sapiens	125-133	
18544087-9	2008	We further examined the effect of CTD on the IL-6 signaling pathway in myeloma cells, and found that CTD inhibited phosphorylation of STAT3 at tyrosine 705 residue as early as 1 h after treatment and down-regulated the expression of the antiapoptotic bcl-xL protein.	Tyrosine	143-151	BCL2 like 1	Homo sapiens	251-257	
17371836-4	2007	Tyrosine phosphorylation of Sam68 by Fyn inverted this effect and favored the Bcl-x(L) splice site selection.	Tyrosine	0-8	BCL2 like 1	Homo sapiens	78-86	
17371836-8	2007	Our results indicate that Sam68 plays a role in the regulation of Bcl-x alternative splicing and that tyrosine phosphorylation of Sam68 by Src-like kinases can switch its role from proapoptotic to antiapoptotic in live cells.	Tyrosine	102-110	BCL2 like 1	Homo sapiens	66-71	
16897757-6	2006	Mitochondrial Bcl-XL is increased in Tyr/Phe-restricted but decreased in Met-restricted cells.	Tyrosine	37-40	BCL2 like 1	Homo sapiens	14-20	
16897757-8	2006	Tyr/Phe restriction also inhibits Bcl-2 and Met restriction inhibits Bcl-XL in mitochondria.	Tyrosine	0-3	BCL2 like 1	Homo sapiens	69-75	
14744023-5	2003	The level of the pro-apoptotic regulator Bax peaked after 6 h and then returned to normal, whereas the level of the anti-apoptotic regulator Bcl-xL, which is presumably induced in order to inhibit apoptosis, started to increase at 6 h, and remained high for 24 h. Phosphorylation of Cdc2 on Tyr-15 greatly increased while p21 rose to a plateau at 8 h. Levels of p53 and Mad2 proteins were unchanged.	Tyrosine	291-294	BCL2 like 1	Homo sapiens	141-147	
10564283-7	1999	Wild-type and a betac mutant lacking tyrosine residues can induce expression of c-myc and bcl-x(L) genes; however, drug sensitivities for activation of these genes differ from those for antiapoptosis activity of GM-CSF, which means that these gene products may be involved yet are inadequate to promote cell survival.	Tyrosine	37-45	BCL2 like 1	Homo sapiens	90-98	
10085098-9	1999	These findings indicate that RAFTK-dependent induction of JNK in response to MMS is sensitive to Bcl-xL, but not to CrmA and p35, by a mechanism that inhibits tyrosine phosphorylation and thereby activation of RAFTK.	Tyrosine	159-167	BCL2 like 1	Homo sapiens	97-103